Вы находитесь на странице: 1из 30

ninth edition TORTORA  FUNKE  CASE

MICROBIOLOGY
an introduction

16 Innate Immunity:
Nonspecific Defenses
of the Host

PowerPoint® Lecture Slide Presentation prepared by Christine L. Case


Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Nonspecific Defenses of the Host

 Susceptibility: Lack of resistance to a disease.


 Immunity: Ability to ward off disease.
 Innate immunity: Defenses against any pathogen.
 Adaptive immunity: Immunity, resistance to a specific
pathogen.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Host Defenses

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.1
Physical Factors

 Skin
 Epidermis consists of tightly packed cells with
 Keratin, a protective protein

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Physical Factors
 Mucous membranes
 Ciliary escalator:
Microbes trapped in mucus
are transported away from
the lungs.
 Lacrimal apparatus:
Washes eye.
 Saliva: Washes microbes off.
 Urine: Flows out.
 Vaginal secretions: Flow out.
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.4a
Chemical Factors

 Fungistatic fatty acid in sebum.


 Low pH (3-5) of skin.
 Lysozyme in perspiration, tears, saliva, and tissue
fluids.
 Low pH (1.2-3.0) of gastric juice.
 Transferrins in blood find iron.
 NO inhibits ATP production.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Normal Microbiota

 Microbial antagonism/competitive exclusion: Normal


microbiota compete with pathogens.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Formed Elements in Blood

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 16.1 (1 of 2)
Formed Elements in Blood

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Table 16.1 (2 of 2)
Differential White Cell Count

 Percentage of each type of white cell in a sample of


100 white blood cells.

Neutrophils 60-70%
Basophils 0.5-1%

Eosinophils 2-4%

Monocytes 3-8%

Lymphocytes 20-25%

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


White Blood Cells
 Neutrophils: Phagocytic
 Basophils: Produce histamine
 Eosinophils: Toxic to parasites and some phagocytosis
 Dendritic cells: Initiate adaptive immune response
 Monocytes: Phagocytic as mature macrophages
 Fixed macrophages in lungs, liver, and bronchi
 Wandering macrophages roam tissues.
 Lymphocytes: Involved in specific immunity.

PLAY Animation: Host Defenses


Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Phagocytosis

 Phago: from Greek,


meaning eat
 Cyte: from Greek,
meaning cell
 Ingestion of microbes
or particles by a cell,
performed by
phagocytes.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.6
Phagocytosis

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.7
Microbial Evasion of Phagocytosis

Inhibit adherence: M protein, Streptococcus pyogenes, S. pneumoniae


capsules
Kill phagocytes: Leukocidins Staphylococcus aureus

Lyse phagocytes: Membrane Listeriamonocytogenes


attack complex
Escape phagosome Shigella

Prevent phagosome-lysosome HIV


fusion
Survive in phagolysosome Coxiella burnetti

PLAY Animation: Phagocytosis


Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Inflammation
 Redness
 Pain
 Heat
 Swelling (edema)
 Acute-phase proteins activated (complement, cytokine,
and kinins)
 Vasodilation (histamine, kinins, prostaglandins, and
leukotrienes)
 Margination and emigration of WBCs
 Tissue repair
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Chemicals Released by Damaged Cells

Histamine Vasodilation, increased permeability


of blood vessels
Kinins Vasodilation, increased permeability
of blood vessels
Prostaglandins Intensity histamine and kinin effect

Leukotrienes Increased permeability of blood vessels,


phagocytic attachment

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Inflammation

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.8a–b
Inflammation

PLAY Animation: Inflammation


Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.8c–d
Fever: Abnormally High Body Temperature

 Hypothalamus normally set at 37°C.


 Gram-negative endotoxin cause phagocytes to release
interleukin–1 (IL–1).
 Hypothalamus releases prostaglandins that reset the
hypothalamus to a high temperature.
 Body increases rate of metabolism and shivering which
raise temperature.
 When IL–1 is eliminated, body temperature falls (crisis).

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Fever

 Advantages  Disadvantages
 Increase transferrins  Tachycardia
 Increase IL–1 activity  Acidosis
 Dehydration

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


The Complement System

 Serum proteins
activated in a
cascade.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.9
Effects of Complement Activation

 Opsonization or
immune adherence:
Enhanced
phagocytosis.
 Membrane attack
complex: Cytolysis.
 Attract phagocytes.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.10
Effects of Complement Activation

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.11
Classical Pathway

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.12
Alternative Pathway

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.13
Lectin Pathway

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.14
Some Bacteria Evade Complement

 Capsules prevent C activation.


 Surface lipid-carbohydrates prevent MAC formation.
 Enzymatic digestion of C5a.

PLAY Animation: The Complement System


Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Interferons (IFNs)

 Alpha IFN and Beta IFN: Cause cells to produce


antiviral proteins that inhibit viral replication.
 Gamma IFN: Causes neutrophils and macrophages
to phagocytize bacteria.

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings


Interferons (IFNs)

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings Figure 16.15
Innate Immunity

 Transferrins  Antimicrobial peptides


 Bind serum iron  Lyse bacterial cells

Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Вам также может понравиться