Вы находитесь на странице: 1из 15


Helicobacter pylori - Wikipedia, the free encyclopedia

Helicobacter pylori
From Wikipedia, the free encyclopedia

Helicobacter pylori (/hlkbktr palra/; H. pylori), previously named Campylobacter pyloridis, is a Gram-negative, microaerophilic bacterium found in the stomach. It was identified in 1982 by Barry Marshall and Robin Warren, who found that it was present in patients with chronic gastritis and gastric ulcers, conditions that were not previously believed to have a microbial cause. It is also linked to the development of duodenal ulcers and stomach cancer. However, over 80 percent of individuals infected with the bacterium are asymptomatic and it has been postulated that it may play an important role in the natural stomach ecology.[1]

Helicobacter pylori infection

Classification and external resources

Immunohistochemical staining of H. pylori from a gastric biopsy ICD-9 041.86 (http://www.icd9data.com/getICD9Code.ashx? icd9=041.86)

DiseasesDB 5702 (http://www.diseasesdatabase.com/ddb5702.htm) MedlinePlus 000229 (http://www.nlm.nih.gov/medlineplus/ency/article/000229.htm) eMedicine MeSH med/962 (http://www.emedicine.com/med/topic962.htm) D016481 (http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?

More than 50% of the world's field=uid&term=D016481) population harbor H. pylori in their upper gastrointestinal tract. Infection is more prevalent in developing countries, and incidence is decreasing in Western countries. H. pylori's helix shape (from which the generic name is derived) is thought to have evolved to penetrate the mucoid lining of the stomach.[2][3]

1 Signs and symptoms 2 Microbiology 2.1 Genome 3 Pathophysiology 4 Diagnosis 5 Prevention 5.1 Vaccines 6 Treatment 7 Prognosis 8 Epidemiology 9 Evolution 10 History 11 References
en.wikipedia.org/wiki/Helicobacter_pylori 1/15


Helicobacter pylori - Wikipedia, the free encyclopedia

12 External links

Signs and symptoms

Over 80% of people infected with H. pylori show no symptoms.[4] Acute infection may appear as an acute gastritis with abdominal pain (stomach ache) or nausea.[5] Where this develops into chronic gastritis, the symptoms, if present, are often those of non-ulcer dyspepsia: stomach pains, nausea, bloating, belching and sometimes vomiting, black stool.[6][7] Individuals infected with H. pylori have a 10 to 20% lifetime risk of developing peptic ulcers and a 1 to 2% risk of acquiring stomach cancer.[8] Inflammation of the pyloric antrum is more likely to lead to duodenal ulcers, while inflammation of the corpus (body of the stomach) is more likely to lead to gastric ulcers and gastric carcinoma.[9] However, it is possible that H. pylori plays a role only in the first stage that leads to common chronic inflammation, but not in further stages leading to carcinogenesis.[3]

H. pylori is a helix-shaped (classified as a curved rod, not spirochaete), Gram-negative bacterium, about 3 micrometres long with a diameter of about 0.5 micrometres. It is microaerophilic; that is, it requires oxygen, but at lower concentration than is found in the atmosphere. It contains a hydrogenase which can be used to obtain energy by oxidizing molecular hydrogen (H2) produced by intestinal bacteria.[10] It produces oxidase, catalase, and urease. It is capable of forming biofilms[11] and can convert from spiral to a possibly viable but nonculturable coccoid form,[12] both likely to favor its survival and be factors in the epidemiology of the bacterium. Helicobacter pylori

Scientific classification Domain: Bacteria Phylum: Proteobacteria Class: Epsilonproteobacteria Order: Campylobacterales Family: Helicobacteraceae Genus: Helicobacter Species: H. pylori Binomial name Helicobacter pylori
(Marshall et al. 1985) Goodwin et al., 1989

Scanning electron micrograph of H. pylori

H. pylori possesses five major outer membrane protein (OMP) families.[13] The largest family includes known and putative adhesins. The other four families include porins, iron transporters, flagellum-associated proteins and proteins of unknown function. Like other typical Gram-negative bacteria, the outer membrane of H. pylori consists of phospholipids and lipopolysaccharide (LPS). The O antigen of LPS may be fucosylated and mimic Lewis blood group antigens found on the gastric epithelium.[13] The outer membrane also contains cholesterol glucosides, which are found in few other bacteria.[13] H. pylori has four to six lophotrichous flagella; all gastric and enterohepatic Helicobacter species are highly motile due to flagella.[14] The characteristic sheathed flagellar filaments of Helicobacter are composed of two copolymerized flagellins, FlaA and FlaB.[15]

en.wikipedia.org/wiki/Helicobacter_pylori 2/15


Helicobacter pylori - Wikipedia, the free encyclopedia

H. pylori consists of a large diversity of strains, and the genomes of three have been completely sequenced.[16][17][18][19][20] The genome of the strain "26695" consists of about 1.7 million base pairs, with some 1,550 genes. The two sequenced strains show large genetic differences, with up to 6% of the nucleotides differing.[18] Study of the H. pylori genome is centered on attempts to understand pathogenesis, the ability of this organism to cause disease. Approximately 29% of the loci are in the "pathogenesis" category of the genome database. Two of sequenced strains have an approximately 40 kb-long Cag pathogenicity island (a common gene sequence believed responsible for pathogenesis) that contains over 40 genes. This pathogenicity island is usually absent from H. pylori strains isolated from humans who are carriers of H. pylori, but remain asymptomatic.[21] The cagA gene codes for one of the major H. pylori virulence proteins. Bacterial strains that have the cagA gene are associated with an ability to cause ulcers.[22] The cagA gene codes for a relatively long (1186 amino acid) protein. The cag pathogenicity island (PAI) has about 30 genes, part of which code for a complex type IV secretion system. The low GC-content of the cag PAI relative to the rest of the Helicobacter genome suggests the island was acquired by horizontal transfer from another bacterial species.[16]

To colonize the stomach, H. pylori must survive the acidic pH of the lumen and use its flagella to burrow into the mucus to reach its niche, close to the stomach's epithelial cell layer.[23] Many bacteria can be found deep in the mucus, which is continuously secreted by mucussecreting cells and removed on the luminal side. To avoid being carried into the lumen, H. pylori senses the pH gradient within the mucus layer by chemotaxis and swims away from the acidic contents of the lumen towards the more neutral pH environment of the epithelial cell surface.[24] H. pylori is also found on the inner surface of the stomach epithelial cells and occasionally inside epithelial cells.[25] It produces adhesins which bind to membrane-associated lipids and carbohydrates and help it adhere to epithelial cells. For example, the adhesin BabA binds to the Lewis b antigen displayed on the surface of stomach epithelial cells.[26] H. pylori produces large amounts of the enzyme urease, molecules of which are localized inside and outside of the bacterium. Urease breaks down urea (which is normally secreted into the stomach) to carbon dioxide and ammonia. The ammonia is converted to ammonium by accepting a proton (H+), which neutralizes gastric acid. The survival of H. pylori in the acidic stomach is dependent on urease. The ammonia produced is toxic to the epithelial cells, and, along with the other products of H. pylori including proteases, vacuolating cytotoxin A (VacA), and certain phospholipases, damages those cells.[27]

Molecular model of H. pylori urease enzyme

Inflammatory processes of H. pylori infections are also mediated by highly disulfide-bridged proteins. Helicobacter cysteine-rich proteins (Hcp), particularly HcpA (hp0211), triggers an immune response through the differentiation of human myeloid Thp1 monocytes into macrophages. In analogy to eukaryotic cytokines, they interfere with host cell functions and change the morphology of monocytes, inducing the expression of the surface marker protein CD11b, phagocytic activity, as well as cell adherence, which are indicative of monocyte differentiation into macrophages.[28]
en.wikipedia.org/wiki/Helicobacter_pylori 3/15


Helicobacter pylori - Wikipedia, the free encyclopedia

Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining. The severity of the inflammation is likely to underlie H. pylori-related diseases.[29] Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances. The type of ulcer that develops depends on the location of chronic gastritis, which occurs at the site of H. pylori colonization.[30] The acidity within the stomach lumen affects the colonization pattern of H. pylori, and therefore ultimately determines whether a duodenal or gastric ulcer will form. In people producing large amounts of acid, H. pylori colonizes the antrum of the stomach to avoid the acid-secreting parietal cells located in the corpus (main body) of the stomach.[13] The inflammatory response to the bacteria induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to the corpus.[31] Gastrin stimulates the parietal cells in the corpus to secrete even more acid into the stomach lumen. Chronically increased gastrin levels eventually cause the number of parietal cells to also increase, further escalating the amount of acid secreted.[32] The increased acid load damages the duodenum, and ulceration may eventually result. In contrast, gastric ulcers are often associated with normal or reduced gastric acid production, suggesting the mechanisms that protect the gastric mucosa are defective.[32] In these patients, H. pylori can also colonize the corpus of the stomach, where the acid-secreting parietal cells are located. However chronic inflammation induced by the bacteria causes further reduction of acid production and, eventually, atrophy of the stomach lining, which may lead to gastric ulcer and increases the risk for stomach cancer.[33] About 50-70% of H. pylori strains in Western countries carry the cag pathogenicity island (cag PAI).[34] Western patients infected with strains carrying the cag PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island.[13] Following attachment of H. pylori to stomach epithelial cells, the type IV secretion system expressed by the cag PAI "injects" the inflammation-inducing agent, peptidoglycan, from their own cell wall into the epithelial cells. The injected peptidoglycan is recognized by the cytoplasmic pattern recognition receptor (immune sensor) Nod1, which then stimulates expression of cytokines that promote inflammation.[35] The type IV secretion apparatus also injects the cag PAI-encoded protein CagA into the stomach's epithelial cells, where it disrupts the cytoskeleton, adherence to adjacent cells, intracellular signaling, cell polarity, and other cellular activities.[36] Once inside the cell, the CagA protein is phosphorylated on tyrosine residues by a host cell membrane-associated tyrosine kinase (TK). CagA then allosterically activates protein tyrosine phosphatase/protooncogene Shp2.[37] Pathogenic strains of H. pylori have been shown to activate the epidermal growth factor receptor (EGFR), a membrane protein with a tyrosine kinase domain. Activation of the EGFR by H. pylori is associated with altered signal transduction and gene expression in host epithelial cells that may contribute to pathogenesis. It has also been suggested that a C-terminal region of the CagA protein (amino acids 8731002) can regulate host cell gene transcription, independent of protein tyrosine phosphorylation.[21][22] There is a great deal of diversity between strains of H. pylori, and the strain with which one is infected is predictive of the outcome. Two related mechanisms by which H. pylori could promote cancer are under investigation. One mechanism involves the enhanced production of free radicals near H. pylori and an increased rate of host cell mutation. The other proposed mechanism has been called a "perigenetic pathway",[38] and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins, such as adhesion proteins. H. pylori has been proposed to induce inflammation and locally high levels of TNF- and/or interleukin 6 (IL-6). According to the proposed perigenetic mechanism, inflammation-associated signaling molecules, such as TNF-, can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in tumor suppressor genes, such as genes that code for cell adhesion proteins.[39]

en.wikipedia.org/wiki/Helicobacter_pylori 4/15


Helicobacter pylori - Wikipedia, the free encyclopedia

Colonization with H. pylori is not a disease in and of itself but a condition associated with a number of disorders of the upper gastrointestinal tract.[13] Testing for H. pylori is recommended if there is peptic ulcer disease, low grade gastric MALT lymphoma, after endoscopic resection of early gastric cancer, if there are first degree relatives with gastric cancer, and in certain cases of dyspepsia,[40] not routinely.[13] Several ways of testing exist. One can test noninvasively for H. pylori infection with a blood antibody test, stool antigen test, or with the carbon urea breath test (in which the patient drinks 14C- or 13C-labelled urea, which the H. pylori colonized on the surface of bacterium metabolizes, producing labelled carbon dioxide that can be regenerative epithelium (image from detected in the breath).[40] However, the most reliable method for Warthin-Starry's silver stain) detecting H. pylori infection is a biopsy check during endoscopy with a rapid urease test, histological examination, and microbial culture. There is also a urine ELISA test with a 96% sensitivity and 79% specificity. None of the test methods are completely failsafe. Even biopsy is dependent on the location of the biopsy. Blood antibody tests, for example, range from 76% to 84% sensitivity. Some drugs can affect H. pylori urease activity and give false negatives with the urea-based tests.[41]

H. pylori is a major cause of certain diseases of the upper gastrointestinal tract. Rising antibiotic resistance increases the need to search for new therapeutic strategies; this might include prevention in form of vaccination.[42] Extensive vaccine studies in mouse models have shown promising results.[43] Researchers are studying different adjuvants, antigens, and routes of immunization to ascertain the most appropriate system of immune protection; however, most of the research only recently moved from animal to human trials.[44] A number of foods may be useful to prevent colonization with H. pylori including: green tea, red wine, broccoli sprouts, garlic, probiotics and flavonoids.[45]

Vaccines against H. pylori could be used as prophylactic vaccines to prevent the infection or as therapeutic vaccines to cure the infection, to improve the eradication success of standard regimens or to reduce the bacterial density in the gastric mucosa and the risk for emergence of antibiotic resistant strains. In recent years, many attempts, using various H. pylori antigens such as urease, CagA, HP-NAP, HspA or combinations, many adjuvants and different routes of immunisation have been made to create vaccines against H. pylori infection. Although some attempts are promising, no effective and safe vaccine against H. pylori is currently available for humans. New directions for immunisation with the use of DNA, living vectors, microspheres etc. are currently under evaluation. The vaccination plan and the groups who should receive vaccination are still to be determined, but the vaccination will be useful, especially in developing countries.[4] An intramuscular vaccine against H. pylori infection is undergoing Phase I clinical trials, and has shown an antibody response against the bacterium. Its clinical usefulness requires further study.[46]

Further information: Helicobacter pylori eradication protocols Once H. pylori is detected in a person with a peptic ulcer, the normal procedure is to eradicate it and allow the ulcer to heal. The standard first-line therapy is a one week "triple therapy" consisting of proton pump inhibitors such as omeprazole and the antibiotics clarithromycin and amoxicillin.[47] Variations of the triple therapy have
en.wikipedia.org/wiki/Helicobacter_pylori 5/15


Helicobacter pylori - Wikipedia, the free encyclopedia

been developed over the years, such as using a different proton pump inhibitor, as with pantoprazole or rabeprazole, or replacing amoxicillin with metronidazole for people who are allergic to penicillin.[48] Such a therapy has revolutionized the treatment of peptic ulcers, and has made a cure to the disease possible; previously, the only option was symptom control using antacids, H2-antagonists or proton pump inhibitors alone.[49][50] An increasing number of infected individuals are found to harbour antibiotic-resistant bacteria. This results in initial treatment failure and requires additional rounds of antibiotic therapy or alternative strategies, such as a quadruple therapy, which adds a bismuth colloid, such as bismuth subsalicylate.[40][51][52] For the treatment of clarithromycin-resistant strains of H. pylori, the use of levofloxacin as part of the therapy has been suggested.[53][54] An article in the American Journal of Clinical Nutrition found evidence that "ingesting lactic acid bacteria exerts a suppressive effect on Helicobacter pylori infection in both animals and humans," noting that "supplementing with Lactobacillus- and Bifidobacterium-containing yogurt (AB-yogurt) was shown to improve the rates of eradication of H. pylori in humans."[55]

H. pylori colonizes the stomach and induces chronic gastritis, a long-lasting inflammation of the stomach. The bacterium persists in the stomach for decades in most people. Most individuals infected by H. pylori will never experience clinical symptoms despite having chronic gastritis. Approximately 10-20% of those colonized by H. pylori will ultimately develop gastric and duodenal ulcers.[13] H. pylori infection is also associated with a 1-2% lifetime risk of stomach cancer and a less than 1% risk of gastric MALT lymphoma.[13] In the absence of treatment, H. pylori infectiononce established in its gastric nicheis widely believed to persist for life.[3] In the elderly, however, it is likely infection can disappear as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. The proportion of acute infections that persist is not known, but several studies that followed the natural history in populations have reported apparent spontaneous elimination.[56][57] Mounting evidence suggests that H. pylori has an important role in protecting from some diseases. The incidence of acid reflux disease, Barrett's esophagus, and esophageal cancer have been rising dramatically at the same time as H. pylori's presence decreases.[58] In 1996, Martin J. Blaser advanced the hypothesis that H. pylori has a beneficial effect: by regulating the acidity of the stomach contents.[31][58] The hypothesis is not universally accepted as several randomized controlled trials failed to demonstrate worsening of acid reflux disease symptoms following eradication of H. pylori.[59][60] Nevertheless, Blaser has refined his view to assert that H. pylori is a member of the normal flora of the stomach.[61] He postulates that the changes in gastric physiology caused by the loss of H. pylori account for the recent increase in incidence of several diseases, including type 2 diabetes, obesity, and asthma.[61][62] His group has recently shown that H. pylori colonization is associated with a lower incidence of childhood asthma.[63]

At least half the world's population are infected by the bacterium, making it the most widespread infection in the world.[64] Actual infection rates vary from nation to nation; the developing world has much higher infection rates than the West (Western Europe, North America, Australasia), where rates are estimated to be around 25%.[64] The age at which this bacterium is acquired seems to influence the possible pathologic outcome of the infection : people infected with it at an early age are likely to develop more intense inflammation that may be followed by
en.wikipedia.org/wiki/Helicobacter_pylori 6/15


Helicobacter pylori - Wikipedia, the free encyclopedia

atrophic gastritis with a higher subsequent risk of gastric ulcer, gastric cancer or both. Acquisition at an older age brings different gastric changes more likely to lead to duodenal ulcer.[3] Infections are usually acquired in early childhood in all countries.[13] However, the infection rate of children in developing nations is higher than in industrialized nations, probably due to poor sanitary conditions. In developed nations it is currently uncommon to find infected children, but the percentage of infected people increases with age, with about 50% infected for those over the age of 60 compared with around 10% between 18 and 30 years.[64] The higher prevalence among the elderly reflects higher infection rates when they were children rather than infection at later ages.[13] Prevalence appears to be higher in African-American and Hispanic populations, most likely due to socioeconomic factors.[65][66] The lower rate of infection in the West is largely attributed to higher hygiene standards and widespread use of antibiotics. Despite high rates of infection in certain areas of the world, the overall frequency of H. pylori infection is declining.[67] However, antibiotic resistance is appearing in H. pylori; there are already many metronidazole- and clarithromycin-resistant strains in most parts of the world.[68] H. pylori is contagious, although the exact route of transmission is not known.[69][70] Person-to-person transmission by either the oral-oral or fecal-oral route is most likely. Consistent with these transmission routes, the bacteria have been isolated from feces, saliva and dental plaque of some infected people. Findings suggest that H. pylori is more easily transmitted via gastric mucous than via saliva[3] Transmission occurs mainly within families in developed nations yet can also be acquired from the community in developing countries.[71] H. pylori may also be transmitted orally by means of fecal matter through the ingestion of waste-tainted water, so a hygienic environment could help decrease the risk of H. pylori infection.[3]

Helicobacter pylori migrated out of Africa along with its human host circa 60,000 years ago.[72] Its subsequent evolution created seven prototypes - Europe (isolated from Europe, the Middle East, India and Iran), NE Africa (from Northeast Africa), Africa1 (from countries in Western Africa and South Africa), Africa2 (from South Africa), Asia2 (from Northern India and among isolates from Bangladesh, Thailand and Malaysia), Sahul (from Australian Aboriginals and Papua New Guineans) and East Asia with the subpopulations E Asia (from East Asians), Maori (from Taiwanese Aboriginals, Melanesians and Polynesians) and Amerind (Native Americans). The precursors of these prototypes have been named ancestral Europe1, ancestral Europe2, ancestral East Asia, ancestral Africa1, ancestral Africa2 and ancestral Sahul. These ancestral prototypes appear to have originated in Africa, Central and East Asia. European and African strains were introduced into the Americas along with its colonisation - both thousands of years ago and more recently - and the slave trade.

See also: Timeline of peptic ulcer disease and Helicobacter pylori Helicobacter pylori was first discovered in the stomachs of patients with gastritis and stomach ulcers in 1982 by Dr. Barry Marshall and Dr. Robin Warren of Perth, Western Australia. At the time, the conventional thinking was that no bacterium can live in the human stomach, as the stomach produced extensive amounts of acid of a strength similar to the acid found in a car battery. Marshall and Warren rewrote the textbooks with reference to what causes gastritis and gastric ulcers. In recognition of their discovery, they were awarded the 2005 Nobel Prize in Physiology or Medicine.[73] German scientists found spiral-shaped bacteria in the lining of the human stomach in 1875, but they were unable to culture it, and the results were eventually forgotten.[58] The Italian researcher Giulio Bizzozero described similarly shaped bacteria living in the acidic environment of the stomach of dogs in 1893.[74] Professor Walery Jaworski of the Jagiellonian University in Krakw investigated sediments of gastric washings obtained from humans in 1899. Among some rod-like bacteria, he also found bacteria with a characteristic spiral shape, which he called Vibrio rugula. He was the first to suggest a possible role of this
en.wikipedia.org/wiki/Helicobacter_pylori 7/15


Helicobacter pylori - Wikipedia, the free encyclopedia

organism in the pathogenesis of gastric diseases. This work was included in the Handbook of Gastric Diseases, but it had little impact, as it was written in Polish.[75] Several small studies conducted in the early 20th century demonstrated the presence of curved rods in the stomach of many patients with peptic ulcers and stomach cancer.[76] Interest in the bacteria waned, however, when an American study published in 1954 failed to observe the bacteria in 1180 stomach biopsies.[77] Interest in understanding the role of bacteria in stomach diseases was rekindled in the 1970s, with the visualization of bacteria in the stomach of gastric ulcer patients.[78] The bacterium had also been observed in 1979, by Australian pathologist Robin Warren, who did further research on it with Australian physician Barry Marshall beginning in 1981. After numerous unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualizing colonies in 1982, when they unintentionally left their Petri dishes incubating for 5 days over the Easter weekend. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food, as had been assumed before.[79] Although there was some skepticism initially, within several years numerous research groups verified the association of H. pylori with gastritis and, to a lesser extent, ulcers.[80] To demonstrate H. pylori caused gastritis and was not merely a bystander, Marshall drank a beaker of H. pylori culture. He became ill with nausea and vomiting several days later. An endoscopy ten days after inoculation revealed signs of gastritis and the presence of H. pylori. These results suggested H. pylori was the causative agent of gastritis. Marshall and Warren went on to demonstrate that antibiotics are effective in the treatment of many cases of gastritis. In 1987, the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers.[81] In 1994, the National Institutes of Health (USA) published an opinion stating most recurrent duodenal and gastric ulcers were caused by H. pylori, and recommended antibiotics be included in the treatment regimen.[82] The bacterium was initially named Campylobacter pyloridis, then renamed C. pylori (pylori being the genitive of pylorus) to correct a Latin grammar error. When 16S ribosomal RNA gene sequencing and other research showed in 1989 that the bacterium did not belong in the genus Campylobacter, it was placed in its own genus, Helicobacter. The genus derived from the ancient Greek hlix/ "spiral" or "coil".[83] The specific epithet pylri means "of the pylorus" or pyloric valve (the circular opening leading from the stomach into the duodenum), from the Ancient Greek word , which means gatekeeper.[83] Recent research states that genetic diversity in H. pylori decreases with geographic distance from East Africa, the birthplace of modern humans. Using the genetic diversity data, the researchers have created simulations that indicate the bacteria seem to have spread from East Africa around 58,000 years ago. Their results indicate modern humans were already infected by H. pylori before their migrations out of Africa, and it has remained associated with human hosts since that time.[84]

1. ^ Blaser, M. J. (2006). "Who are we? Indigenous microbes and the ecology of human diseases" (http://www.nature.com/embor/journal/v7/n10/pdf/7400812.pdf) . EMBO Reports 7 (10): 95660. doi:10.1038/sj.embor.7400812 (http://dx.doi.org/10.1038%2Fsj.embor.7400812) . PMC 1618379 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1618379/?tool=pmcentrez) . PMID 17016449 (//www.ncbi.nlm.nih.gov/pubmed/17016449) . http://www.nature.com/embor/journal/v7/n10/pdf/7400812.pdf. 2. ^ Yamaoka, Yoshio (2008). Helicobacter pylori: Molecular Genetics and Cellular Biology. Caister Academic Pr. ISBN 1-904455-31-X. 3. ^ a b c d e f Brown LM (2000). "Helicobacter pylori: epidemiology and routes of transmission" (http://epirev.oxfordjournals.org/content/22/2/283.full.pdf) . Epidemiol Rev 22 (2): 28397. PMID 11218379 (//www.ncbi.nlm.nih.gov/pubmed/11218379) . http://epirev.oxfordjournals.org/content/22/2/283.full.pdf.




Helicobacter pylori - Wikipedia, the free encyclopedia

4. 5.

6. 7. 8.









17. 18.




(//www.ncbi.nlm.nih.gov/pubmed/11218379) . http://epirev.oxfordjournals.org/content/22/2/283.full.pdf. ^ a b Boyanova, L (editor) (2011). Helicobacter pylori. Caister Academic Press. ISBN 978-1-904455-84-4. ^ Butcher, Graham P. (2003). Gastroenterology: An Illustrated Colour Text (http://books.google.com/? id=yx22Lgl1uYkC&pg=PAx25v=onepage&q) . Elsevier Health Sciences. p. 25. ISBN 0-443-06215-3. http://books.google.com/?id=yx22Lgl1uYkC&pg=PAx25v=onepage&q. Retrieved 2011-09-06. ^ Butcher (2003), pp. 24-5 ^ Ryan, Kenneth (2010). Sherris Medical Microbiology. McGraw-Hill. pp. 573 and 576. ISBN 978-0-07160402-4. ^ Kusters JG, van Vliet AH, Kuipers EJ (July 2006). "Pathogenesis of Helicobacter pylori Infection" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1539101) . Clin Microbiol Rev 19 (3): 44990. doi:10.1128/CMR.00054-05 (http://dx.doi.org/10.1128%2FCMR.00054-05) . PMC 1539101 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1539101/?tool=pmcentrez) . PMID 16847081 (//www.ncbi.nlm.nih.gov/pubmed/16847081) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1539101. ^ Suerbaum S, Michetti P (October 2002). "Helicobacter pylori infection". N. Engl. J. Med. 347 (15): 117586. doi:10.1056/NEJMra020542 (http://dx.doi.org/10.1056%2FNEJMra020542) . PMID 12374879 (//www.ncbi.nlm.nih.gov/pubmed/12374879) . ^ Olson JW, Maier RJ (November 2002). "Molecular hydrogen as an energy source for Helicobacter pylori". Science 298 (5599): 178890. doi:10.1126/science.1077123 (http://dx.doi.org/10.1126%2Fscience.1077123) . PMID 12459589 (//www.ncbi.nlm.nih.gov/pubmed/12459589) . ^ Stark RM, Gerwig GJ, Pitman RS et al. (February 1999). "Biofilm formation by Helicobacter pylori". Lett Appl Microbiol 28 (2): 1216. doi:10.1046/j.1365-2672.1999.00481.x (http://dx.doi.org/10.1046%2Fj.13652672.1999.00481.x) . PMID 10063642 (//www.ncbi.nlm.nih.gov/pubmed/10063642) . ^ Chan WY, Hui PK, Leung KM, Chow J, Kwok F, Ng CS (October 1994). "Coccoid forms of Helicobacter pylori in the human stomach". Am J Clin Pathol 102 (4): 5037. PMID 7524304 (//www.ncbi.nlm.nih.gov/pubmed/7524304) . ^ a b c d e f g h i j k Kusters JG, van Vliet AH, Kuipers EJ (July 2006). "Pathogenesis of Helicobacter pylori Infection" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1539101) . Clin Microbiol Rev 19 (3): 44990. doi:10.1128/CMR.00054-05 (http://dx.doi.org/10.1128%2FCMR.00054-05) . PMC 1539101 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1539101/?tool=pmcentrez) . PMID 16847081 (//www.ncbi.nlm.nih.gov/pubmed/16847081) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1539101. ^ Josenhans C, Eaton KA, Thevenot T, Suerbaum S (August 2000). "Switching of Flagellar Motility in Helicobacter pylori by Reversible Length Variation of a Short Homopolymeric Sequence Repeat in fliP, a Gene Encoding a Basal Body Protein" (//www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=98385) . Infect Immun 68 (8): 4598603. doi:10.1128/IAI.68.8.4598-4603.2000 (http://dx.doi.org/10.1128%2FIAI.68.8.4598-4603.2000) . PMC 98385 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC98385/?tool=pmcentrez) . PMID 10899861 (//www.ncbi.nlm.nih.gov/pubmed/10899861) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=98385. ^ Rust M, Schweinitzer T, Josenhans C (2008). "Helicobacter Flagella, Motility and Chemotaxis" (http://www.horizonpress.com/hpl2) . In Yamaoka Y. Helicobacter pylori: Molecular Genetics and Cellular Biology. Caister Academic Press. ISBN 1-904455-31-X. http://www.horizonpress.com/hpl2. ^ a b Tomb JF, White O, Kerlavage AR et al. (August 1997). "The complete genome sequence of the gastric pathogen Helicobacter pylori". Nature 388 (6642): 53947. doi:10.1038/41483 (http://dx.doi.org/10.1038%2F41483) . PMID 9252185 (//www.ncbi.nlm.nih.gov/pubmed/9252185) . ^ "Genome information for the H. pylori 26695 and J99 strains" (http://genolist.pasteur.fr/PyloriGene) . Institut Pasteur. 2002. http://genolist.pasteur.fr/PyloriGene. Retrieved 2008-09-01. ^ a b "Helicobacter pylori 26695, complete genome" (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? db=genome&cmd=Retrieve&dopt=Overview&list_uids=128) . National Center for Biotechnology Information. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genome&cmd=Retrieve&dopt=Overview&list_uids=128. Retrieved 2008-09-01. ^ "Helicobacter pylori J99, complete genome" (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? db=genome&cmd=Retrieve&dopt=Overview&list_uids=139) . National Center for Biotechnology Information. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=genome&cmd=Retrieve&dopt=Overview&list_uids=139. Retrieved 2008-09-01. ^ Oh JD, Kling-Bckhed H, Giannakis M et al. (June 2006). "The complete genome sequence of a chronic



Helicobacter pylori - Wikipedia, the free encyclopedia

20. ^ Oh JD, Kling-Bckhed H, Giannakis M et al. (June 2006). "The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1480403) . Proc Natl Acad Sci U.S.A. 103 (26): 999910004. doi:10.1073/pnas.0603784103 (http://dx.doi.org/10.1073%2Fpnas.0603784103) . PMC 1480403 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1480403/?tool=pmcentrez) . PMID 16788065 (//www.ncbi.nlm.nih.gov/pubmed/16788065) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1480403. 21. ^ a b Baldwin DN, Shepherd B, Kraemer P et al. (February 2007). "Identification of Helicobacter pylori Genes That Contribute to Stomach Colonization" (//www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1828534) . Infect Immun 75 (2): 100516. doi:10.1128/IAI.01176-06 (http://dx.doi.org/10.1128%2FIAI.01176-06) . PMC 1828534 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1828534/?tool=pmcentrez) . PMID 17101654 (//www.ncbi.nlm.nih.gov/pubmed/17101654) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1828534. 22. ^ a b Broutet N, Marais A, Lamouliatte H et al. (April 2001). "cagA Status and Eradication Treatment Outcome of Anti-Helicobacter pylori Triple Therapies in Patients with Nonulcer Dyspepsia" (http://jcm.asm.org/content/39/4/1319.full.pdf) . J Clin Microbiol 39 (4): 131922. doi:10.1128/JCM.39.4.1319-1322.2001 (http://dx.doi.org/10.1128%2FJCM.39.4.1319-1322.2001) . PMC 87932 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC87932/?tool=pmcentrez) . PMID 11283049 (//www.ncbi.nlm.nih.gov/pubmed/11283049) . http://jcm.asm.org/content/39/4/1319.full.pdf. 23. ^ Amieva MR, El-Omar EM (January 2008). "Host-bacterial interactions in Helicobacter pylori infection". Gastroenterology 134 (1): 30623. doi:10.1053/j.gastro.2007.11.009 (http://dx.doi.org/10.1053%2Fj.gastro.2007.11.009) . PMID 18166359 (//www.ncbi.nlm.nih.gov/pubmed/18166359) . 24. ^ Schreiber S, Konradt M, Groll C et al. (April 2004). "The spatial orientation of Helicobacter pylori in the gastric mucus" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=387367) . Proc. Natl. Acad. Sci. U.S.A. 101 (14): 50249. doi:10.1073/pnas.0308386101 (http://dx.doi.org/10.1073%2Fpnas.0308386101) . PMC 387367 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC387367/?tool=pmcentrez) . PMID 15044704 (//www.ncbi.nlm.nih.gov/pubmed/15044704) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=387367. 25. ^ Petersen AM, Krogfelt KA (May 2003). "Helicobacter pylori: an invading microorganism? A review". FEMS Immunol. Med. Microbiol. 36 (3): 11726. doi:10.1016/S0928-8244(03)00020-8 (http://dx.doi.org/10.1016%2FS0928-8244%2803%2900020-8) . PMID 12738380 (//www.ncbi.nlm.nih.gov/pubmed/12738380) . 26. ^ Ilver D, Arnqvist A, Ogren J et al. (January 1998). "Helicobacter pylori adhesin binding fucosylated histoblood group antigens revealed by retagging". Science 279 (5349): 3737. doi:10.1126/science.279.5349.373 (http://dx.doi.org/10.1126%2Fscience.279.5349.373) . PMID 9430586 (//www.ncbi.nlm.nih.gov/pubmed/9430586) . 27. ^ Smoot DT (December 1997). "How does Helicobacter pylori cause mucosal damage? Direct mechanisms". Gastroenterology 113 (6 Suppl): S314; discussion S50. PMID 9394757 (//www.ncbi.nlm.nih.gov/pubmed/9394757) . 28. ^ Dumrese C, Slomianka L, Ziegler U et al. (May 2009). "The secreted Helicobacter cysteine-rich protein A causes adherence of human monocytes and differentiation into a macrophage-like phenotype" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2764743) . FEBS Letters 583 (10): 163743. doi:10.1016/j.febslet.2009.04.027 (http://dx.doi.org/10.1016%2Fj.febslet.2009.04.027) . PMC 2764743 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC2764743/?tool=pmcentrez) . PMID 19393649 (//www.ncbi.nlm.nih.gov/pubmed/19393649) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=2764743. 29. ^ Shiotani A, Graham DY (November 2002). "Pathogenesis and therapy of gastric and duodenal ulcer disease". Med. Clin. North Am. 86 (6): 144766, viii. doi:10.1016/S0025-7125(02)00083-4 (http://dx.doi.org/10.1016%2FS0025-7125%2802%2900083-4) . PMID 12510460 (//www.ncbi.nlm.nih.gov/pubmed/12510460) . 30. ^ Dixon MF (February 2000). "Patterns of inflammation linked to ulcer disease". Baillieres Best Pract Res Clin Gastroenterol 14 (1): 2740. doi:10.1053/bega.1999.0057 (http://dx.doi.org/10.1053%2Fbega.1999.0057) . PMID 10749087 (//www.ncbi.nlm.nih.gov/pubmed/10749087) . 31. ^ a b Blaser MJ, Atherton JC (February 2004). "Helicobacter pylori persistence: biology and disease"
en.wikipedia.org/wiki/Helicobacter_pylori 10/15



31. ^ a b Blaser MJ, Atherton JC (February 2004). "Helicobacter pylori persistence: biology and disease" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=324548) . J. Clin. Invest. 113 (3): 32133. doi:10.1172/JCI20925 (http://dx.doi.org/10.1172%2FJCI20925) . PMC 324548 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC324548/?tool=pmcentrez) . PMID 14755326 (//www.ncbi.nlm.nih.gov/pubmed/14755326) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=324548. 32. ^ a b Schubert ML, Peura DA (June 2008). "Control of gastric acid secretion in health and disease". Gastroenterology 134 (7): 184260. doi:10.1053/j.gastro.2008.05.021 (http://dx.doi.org/10.1053%2Fj.gastro.2008.05.021) . PMID 18474247 (//www.ncbi.nlm.nih.gov/pubmed/18474247) . 33. ^ Suerbaum S, Michetti P (October 2002). "Helicobacter pylori infection". N. Engl. J. Med. 347 (15): 1175 86. doi:10.1056/NEJMra020542 (http://dx.doi.org/10.1056%2FNEJMra020542) . PMID 12374879 (//www.ncbi.nlm.nih.gov/pubmed/12374879) . 34. ^ Peek RM, Crabtree JE (January 2006). "Helicobacter infection and gastric neoplasia". J. Pathol. 208 (2): 23348. doi:10.1002/path.1868 (http://dx.doi.org/10.1002%2Fpath.1868) . PMID 16362989 (//www.ncbi.nlm.nih.gov/pubmed/16362989) . 35. ^ Viala J, Chaput C, Boneca IG et al. (November 2004). "Nod1 responds to peptidoglycan delivered by the Helicobacter pylori cag pathogenicity island". Nat. Immunol. 5 (11): 116674. doi:10.1038/ni1131 (http://dx.doi.org/10.1038%2Fni1131) . PMID 15489856 (//www.ncbi.nlm.nih.gov/pubmed/15489856) . 36. ^ Backert S, Selbach M (August 2008). "Role of type IV secretion in Helicobacter pylori pathogenesis". Cell. Microbiol. 10 (8): 157381. doi:10.1111/j.1462-5822.2008.01156.x (http://dx.doi.org/10.1111%2Fj.14625822.2008.01156.x) . PMID 18410539 (//www.ncbi.nlm.nih.gov/pubmed/18410539) . 37. ^ Hatakeyama, M (Sep. 2004). "Oncogenic mechanisms of the Helicobacter pylori CagA protein". Nat Rev Cancer (United States) 4 (9): 68894. doi:10.1038/nrc1433 (http://dx.doi.org/10.1038%2Fnrc1433) . PMID 15343275 (//www.ncbi.nlm.nih.gov/pubmed/15343275) . 38. ^ Tsuji S, Kawai N, Tsujii M, Kawano S, Hori M (July 2003). "Review article: inflammation-related promotion of gastrointestinal carcinogenesis--a perigenetic pathway". Aliment. Pharmacol. Ther. 18 Suppl 1: 829. doi:10.1046/j.1365-2036.18.s1.22.x (http://dx.doi.org/10.1046%2Fj.1365-2036.18.s1.22.x) . PMID 12925144 (//www.ncbi.nlm.nih.gov/pubmed/12925144) . 39. ^ Suganuma M, Yamaguchi K, Ono Y et al. (July 2008). "TNF--inducing protein, a carcinogenic factor secreted from H. pylori, enters gastric cancer cells". Int. J. Cancer 123 (1): 11722. doi:10.1002/ijc.23484 (http://dx.doi.org/10.1002%2Fijc.23484) . PMID 18412243 (//www.ncbi.nlm.nih.gov/pubmed/18412243) . 40. ^ a b c Stenstrm B, Mendis A, Marshall B (August 2008). "Helicobacter pylori - The latest in diagnosis and treatment". Aust Fam Physician 37 (8): 60812. PMID 18704207 (//www.ncbi.nlm.nih.gov/pubmed/18704207) . 41. ^ Logan RP, Walker MM (October 2001). "Epidemiology and diagnosis of Helicobacter pylori infection" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1121445) . BMJ 323 (7318): 9202. doi:10.1136/bmj.323.7318.920 (http://dx.doi.org/10.1136%2Fbmj.323.7318.920) . PMC 1121445 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1121445/?tool=pmcentrez) . PMID 11668141 (//www.ncbi.nlm.nih.gov/pubmed/11668141) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1121445. 42. ^ Selgrad M, Malfertheiner P (June 2008). "New strategies for Helicobacter pylori eradication". Curr Opin Pharmacol 8 (5): 5937. doi:10.1016/j.coph.2008.04.010 (http://dx.doi.org/10.1016%2Fj.coph.2008.04.010) . PMID 18555746 (//www.ncbi.nlm.nih.gov/pubmed/18555746) . 43. ^ Hoffelner H, Rieder G, Haas R (January 2008). "Helicobacter pylori vaccine development: optimisation of strategies and importance of challenging strain and animal model". Int. J. Med. Microbiol. 298 (12): 1519. doi:10.1016/j.ijmm.2007.07.006 (http://dx.doi.org/10.1016%2Fj.ijmm.2007.07.006) . PMID 17714988 (//www.ncbi.nlm.nih.gov/pubmed/17714988) . 44. ^ Kabir S (April 2007). "The current status of Helicobacter pylori vaccines: a review". Helicobacter 12 (2): 89 102. doi:10.1111/j.1523-5378.2007.00478.x (http://dx.doi.org/10.1111%2Fj.1523-5378.2007.00478.x) . PMID 17309745 (//www.ncbi.nlm.nih.gov/pubmed/17309745) . 45. ^ Lee, S. .; Shin, Y. .; Hahm, K. . (2008). "Phytoceuticals: mighty but ignored weapons against Helicobacter pylori infection". Journal of digestive diseases 9 (3): 129139. doi:10.1111/j.1751-2980.2008.00334.x (http://dx.doi.org/10.1111%2Fj.1751-2980.2008.00334.x) . PMID 18956590 (//www.ncbi.nlm.nih.gov/pubmed/18956590) . 46. ^ Malfertheiner P, Schultze V, Rosenkranz B et al. (May 2008). "Safety and Immunogenicity of an Intramuscular Helicobacter pylori Vaccine in Noninfected Volunteers: A Phase I Study". Gastroenterology 135

Helicobacter pylori - Wikipedia, the free encyclopedia
















Intramuscular Helicobacter pylori Vaccine in Noninfected Volunteers: A Phase I Study". Gastroenterology 135 (3): 78795. doi:10.1053/j.gastro.2008.05.054 (http://dx.doi.org/10.1053%2Fj.gastro.2008.05.054) . PMID 18619971 (//www.ncbi.nlm.nih.gov/pubmed/18619971) . ^ Malfertheiner, P; Megraud, F; O'Morain, CA; Atherton, J; Axon, AT; Bazzoli, F; Gensini, GF; Gisbert, JP; Graham, DY; Rokkas, T; El-Omar, EM; Kuipers, EJ; European Helicobacter Study, Group (2012 May). "Management of Helicobacter pylori infection--the Maastricht IV/ Florence Consensus Report.". Gut 61 (5): 646-64. PMID 22491499 (//www.ncbi.nlm.nih.gov/pubmed/22491499) . ^ Malfertheiner P, Megraud F, O'Morain C et al. (June 2007). "Current concepts in the management of Helicobacter pylori infection: the Maastricht III Consensus Report" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1954853) . Gut 56 (6): 77281. doi:10.1136/gut.2006.101634 (http://dx.doi.org/10.1136%2Fgut.2006.101634) . PMC 1954853 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1954853/?tool=pmcentrez) . PMID 17170018 (//www.ncbi.nlm.nih.gov/pubmed/17170018) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1954853. ^ Rauws EA, Tytgat GN (May 1990). "Cure of duodenal ulcer associated with eradication of Helicobacter pylori". Lancet 335 (8700): 12335. doi:10.1016/0140-6736(90)91301-P (http://dx.doi.org/10.1016%2F01406736%2890%2991301-P) . PMID 1971318 (//www.ncbi.nlm.nih.gov/pubmed/1971318) . ^ Graham DY, Lew GM, Evans DG, Evans DJ, Klein PD (August 1991). "Effect of triple therapy (antibiotics plus bismuth) on duodenal ulcer healing. A randomized controlled trial". Ann. Intern. Med. 115 (4): 2669. PMID 1854110 (//www.ncbi.nlm.nih.gov/pubmed/1854110) . ^ Fischbach L, Evans EL (August 2007). "Meta-analysis: the effect of antibiotic resistance status on the efficacy of triple and quadruple first-line therapies for Helicobacter pylori". Aliment. Pharmacol. Ther. 26 (3): 34357. doi:10.1111/j.1365-2036.2007.03386.x (http://dx.doi.org/10.1111%2Fj.1365-2036.2007.03386.x) . PMID 17635369 (//www.ncbi.nlm.nih.gov/pubmed/17635369) . ^ Graham DY, Shiotani A (June 2008). "Newer concepts regarding resistance in the treatment Helicobacter pylori infections" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2841357) . Nat Clin Pract Gastroenterol Hepatol 5 (6): 32131. doi:10.1038/ncpgasthep1138 (http://dx.doi.org/10.1038%2Fncpgasthep1138) . PMC 2841357 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC2841357/?tool=pmcentrez) . PMID 18446147 (//www.ncbi.nlm.nih.gov/pubmed/18446147) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=2841357. ^ Perna F, Zullo A, Ricci C, Hassan C, Morini S, Vaira D (November 2007). "Levofloxacin-based triple therapy for Helicobacter pylori re-treatment: role of bacterial resistance". Dig Liver Dis 39 (11): 10015. doi:10.1016/j.dld.2007.06.016 (http://dx.doi.org/10.1016%2Fj.dld.2007.06.016) . PMID 17889627 (//www.ncbi.nlm.nih.gov/pubmed/17889627) . ^ Hsu PI, Wu DC, Chen A et al. (June 2008). "Quadruple rescue therapy for Helicobacter pylori infection after two treatment failures". Eur. J. Clin. Invest. 38 (6): 4049. doi:10.1111/j.1365-2362.2008.01951.x (http://dx.doi.org/10.1111%2Fj.1365-2362.2008.01951.x) . PMID 18435764 (//www.ncbi.nlm.nih.gov/pubmed/18435764) . ^ Wang KY, Li SN, Liu CS et al. (September 2004). "Effects of ingesting Lactobacillus- and Bifidobacteriumcontaining yogurt in subjects with colonized Helicobacter pylori" (http://www.ajcn.org/content/80/3/737.full.pdf) . The American Journal of Clinical Nutrition 80 (3): 73741. PMID 15321816 (//www.ncbi.nlm.nih.gov/pubmed/15321816) . http://www.ajcn.org/content/80/3/737.full.pdf. ^ Goodman KJ, O'rourke K, Day RS et al. (December 2005). "Dynamics of Helicobacter pylori infection in a US-Mexico cohort during the first two years of life". Int J Epidemiol 34 (6): 134855. doi:10.1093/ije/dyi152 (http://dx.doi.org/10.1093%2Fije%2Fdyi152) . PMID 16076858 (//www.ncbi.nlm.nih.gov/pubmed/16076858) . ^ Goodman KJ, Cockburn M (March 2001). "The role of epidemiology in understanding the health effects of Helicobacter pylori". Epidemiology 12 (2): 26671. doi:10.1097/00001648-200103000-00023 (http://dx.doi.org/10.1097%2F00001648-200103000-00023) . PMID 11246592 (//www.ncbi.nlm.nih.gov/pubmed/11246592) . ^ a b c Blaser MJ (February 2005). "An endangered species in the stomach". Sci. Am. 292 (2): 3845. doi:10.1038/scientificamerican0205-38 (http://dx.doi.org/10.1038%2Fscientificamerican0205-38) . PMID 15715390 (//www.ncbi.nlm.nih.gov/pubmed/15715390) . ^ Graham DY, Yamaoka Y, Malaty HM (November 2007). "Contemplating the Future without Helicobacter pylori and the Dire Consequences Hypothesis" (//www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=3128250) . Helicobacter 12 Suppl 2 (Suppl 2): 648. doi:10.1111/j.152312/15

Helicobacter pylori - Wikipedia, the free encyclopedia







64. 65.




69. 70. 71.

72. 73. 74.



tool=pmcentrez&artid=3128250) . Helicobacter 12 Suppl 2 (Suppl 2): 648. doi:10.1111/j.15235378.2007.00566.x (http://dx.doi.org/10.1111%2Fj.1523-5378.2007.00566.x) . PMC 3128250 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC3128250/?tool=pmcentrez) . PMID 17991179 (//www.ncbi.nlm.nih.gov/pubmed/17991179) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=3128250. ^ Delaney B, McColl K (August 2005). "Review article: Helicobacter pylori and gastro-oesophageal reflux disease". Aliment. Pharmacol. Ther. 22 Suppl 1: 3240. doi:10.1111/j.1365-2036.2005.02607.x (http://dx.doi.org/10.1111%2Fj.1365-2036.2005.02607.x) . PMID 16042657 (//www.ncbi.nlm.nih.gov/pubmed/16042657) . ^ a b Blaser MJ (October 2006). "Who are we? Indigenous microbes and the ecology of human diseases" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1618379) . EMBO Reports 7 (10): 95660. doi:10.1038/sj.embor.7400812 (http://dx.doi.org/10.1038%2Fsj.embor.7400812) . PMC 1618379 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1618379/?tool=pmcentrez) . PMID 17016449 (//www.ncbi.nlm.nih.gov/pubmed/17016449) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1618379. ^ Blaser MJ, Chen Y, Reibman J (May 2008). "Does Helicobacter pylori protect against asthma and allergy?". Gut 57 (5): 5617. doi:10.1136/gut.2007.133462 (http://dx.doi.org/10.1136%2Fgut.2007.133462) . PMID 18194986 (//www.ncbi.nlm.nih.gov/pubmed/18194986) . ^ Chen Y, Blaser MJ (August 2008). "Helicobacter pylori colonization is inversely associated with childhood asthma". J. Infect. Dis. 198 (4): 55360. doi:10.1086/590158 (http://dx.doi.org/10.1086%2F590158) . PMID 18598192 (//www.ncbi.nlm.nih.gov/pubmed/18598192) . ^ a b c Pounder RE, Ng D (1995). "The prevalence of Helicobacter pylori infection in different countries". Aliment. Pharmacol. Ther. 9 Suppl 2: 339. PMID 8547526 (//www.ncbi.nlm.nih.gov/pubmed/8547526) . ^ Smoak BL, Kelley PW, Taylor DN (March 1994). "Seroprevalence of Helicobacter pylori infections in a cohort of US Army recruits". Am. J. Epidemiol. 139 (5): 5139. PMID 8154475 (//www.ncbi.nlm.nih.gov/pubmed/8154475) . ^ Everhart JE, Kruszon-Moran D, Perez-Perez GI, Tralka TS, McQuillan G (April 2000). "Seroprevalence and ethnic differences in Helicobacter pylori infection among adults in the United States". J. Infect. Dis. 181 (4): 135963. doi:10.1086/315384 (http://dx.doi.org/10.1086%2F315384) . PMID 10762567 (//www.ncbi.nlm.nih.gov/pubmed/10762567) . ^ Malaty HM (2007). "Epidemiology of Helicobacter pylori infection". Best Pract Res Clin Gastroenterol 21 (2): 20514. doi:10.1016/j.bpg.2006.10.005 (http://dx.doi.org/10.1016%2Fj.bpg.2006.10.005) . PMID 17382273 (//www.ncbi.nlm.nih.gov/pubmed/17382273) . ^ Mgraud F (September 2004). "H pylori antibiotic resistance: prevalence, importance, and advances in testing" (//www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1774187) . Gut 53 (9): 1374 84. doi:10.1136/gut.2003.022111 (http://dx.doi.org/10.1136%2Fgut.2003.022111) . PMC 1774187 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1774187/?tool=pmcentrez) . PMID 15306603 (//www.ncbi.nlm.nih.gov/pubmed/15306603) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1774187. ^ Mgraud F (1995). "Transmission of Helicobacter pylori: faecal-oral versus oral-oral route". Aliment. Pharmacol. Ther. 9 Suppl 2: 8591. PMID 8547533 (//www.ncbi.nlm.nih.gov/pubmed/8547533) . ^ Cave DR (May 1996). "Transmission and epidemiology of Helicobacter pylori". Am. J. Med. 100 (5A): 12S 17S; discussion 17S18S. PMID 8644777 (//www.ncbi.nlm.nih.gov/pubmed/8644777) . ^ Delport W, van der Merwe SW (2007). "The transmission of Helicobacter pylori: the effects of analysis method and study population on inference". Best Pract Res Clin Gastroenterol 21 (2): 21536. doi:10.1016/j.bpg.2006.10.001 (http://dx.doi.org/10.1016%2Fj.bpg.2006.10.001) . PMID 17382274 (//www.ncbi.nlm.nih.gov/pubmed/17382274) . ^ Correa P, Piazuelo MB (2012) Evolutionary History of the Helicobacter pylori Genome: Implications for Gastric Carcinogenesis. Gut Liver 6(1):21-28 ^ "The Nobel Prize in Physiology or Medicine 2005" (http://nobelprize.org/medicine/laureates/2005/index.html) . http://nobelprize.org/medicine/laureates/2005/index.html. Retrieved 2008-08-02. ^ Bizzozero G (1893). "Ueber die schlauchfrmigen Drsen des Magendarmkanals und die Beziehungen ihres Epitheles zu dem Oberflchenepithel der Schleimhaut". Archiv fr mikroskopische Anatomie 42: 82152. doi:10.1007/BF02975307 (http://dx.doi.org/10.1007%2FBF02975307) . ^ Konturek JW (December 2003). "Discovery by Jaworski of Helicobacter pylori and its pathogenetic role in peptic ulcer, gastritis and gastric cancer" (http://web.archive.org/web/20040930111720/http://www.jpp.krakow.pl/journal/archive/1203_s3/pdf/23_1203

Helicobacter pylori - Wikipedia, the free encyclopedia




77. 78.





83. 84.

(http://web.archive.org/web/20040930111720/http://www.jpp.krakow.pl/journal/archive/1203_s3/pdf/23_1203 _s3_article.pdf) (PDF). J. Physiol. Pharmacol. 54 Suppl 3: 2341. PMID 15075463 (//www.ncbi.nlm.nih.gov/pubmed/15075463) . Archived from the original (http://www.jpp.krakow.pl/journal/archive/1203_s3/pdf/23_1203_s3_article.pdf) on September 30, 2004. http://web.archive.org/web/20040930111720/http://www.jpp.krakow.pl/journal/archive/1203_s3/pdf/23_1203_ s3_article.pdf. Retrieved 2008-08-25. ^ Egan BJ, O'Morain CA (2007). "A historical perspective of Helicobacter gastroduodenitis and its complications". Best Pract Res Clin Gastroenterol 21 (2): 33546. doi:10.1016/j.bpg.2006.12.002 (http://dx.doi.org/10.1016%2Fj.bpg.2006.12.002) . PMID 17382281 (//www.ncbi.nlm.nih.gov/pubmed/17382281) . ^ Palmer ED (August 1954). "Investigation of the gastric mucosa spirochetes of the human". Gastroenterology 27 (2): 21820. PMID 13183283 (//www.ncbi.nlm.nih.gov/pubmed/13183283) . ^ Steer HW (August 1975). "Ultrastructure of cell migration through the gastric epithelium and its relationship to bacteria" (http://jcp.bmj.com/content/28/8/639.long) (PDF). J. Clin. Pathol. 28 (8): 63946. doi:10.1136/jcp.28.8.639 (http://dx.doi.org/10.1136%2Fjcp.28.8.639) . PMC 475793 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC475793/?tool=pmcentrez) . PMID 1184762 (//www.ncbi.nlm.nih.gov/pubmed/1184762) . http://jcp.bmj.com/content/28/8/639.long. ^ Marshall BJ, Warren JR (June 1984). "Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration". Lancet 1 (8390): 13115. doi:10.1016/S0140-6736(84)91816-6 (http://dx.doi.org/10.1016%2FS0140-6736%2884%2991816-6) . PMID 6145023 (//www.ncbi.nlm.nih.gov/pubmed/6145023) . ^ Atwood IV KC (2004). "Bacteria, Ulcers, and Ostracism? H. pylori and the making of a myth" (http://www.csicop.org/si/show/bacteria_ulcers_and_ostracism_h._pylori_and_the_making_of_a_myth/) . http://www.csicop.org/si/show/bacteria_ulcers_and_ostracism_h._pylori_and_the_making_of_a_myth/. Retrieved 2008-08-02. ^ Borody TJ, Cole P, Noonan S et al. (October 1989). "Recurrence of duodenal ulcer and Campylobacter pylori infection after eradication". Med. J. Aust. 151 (8): 4315. PMID 2687668 (//www.ncbi.nlm.nih.gov/pubmed/2687668) . ^ "Helicobacter pylori in peptic ulcer disease" (http://consensus.nih.gov/1994/1994HelicobacterPyloriUlcer094html.htm) . NIH Consensus Statement Online Jan 79;12(1):123. http://consensus.nih.gov/1994/1994HelicobacterPyloriUlcer094html.htm. Retrieved 200412-21. ^ a b Liddell HG and Scott R (1966). A Lexicon: Abridged from Liddell and Scott's Greek-English Lexicon. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-910207-4. ^ Linz B, Balloux F, Moodley Y et al. (February 2007). "An African origin for the intimate association between humans and Helicobacter pylori" (//www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1847463) . Nature 445 (7130): 9158. doi:10.1038/nature05562 (http://dx.doi.org/10.1038%2Fnature05562) . PMC 1847463 (//www.ncbi.nlm.nih.gov/pmc/articles/PMC1847463/?tool=pmcentrez) . PMID 17287725 (//www.ncbi.nlm.nih.gov/pubmed/17287725) . //www.pubmedcentral.nih.gov/articlerender.fcgi? tool=pmcentrez&artid=1847463.

Helicobacter pylori - Wikipedia, the free encyclopedia

External links
Information on tests for H. pylori (http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0015937/) from the National Institutes of Health Retrieved from "http://en.wikipedia.org/w/index.php?title=Helicobacter_pylori&oldid=505771356" Categories: Conditions diagnosed by stool test Gastroenterology Gram-negative bacteria IARC Group 1 carcinogens Proteobacteria This page was last modified on 17 August 2012 at 20:51. Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may
en.wikipedia.org/wiki/Helicobacter_pylori 14/15


Helicobacter pylori - Wikipedia, the free encyclopedia

apply. See Terms of use for details. Wikipedia is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization.