Secretory Leukocyte Protease Inhibitor

Regulates Human Periodontal Ligament Cell

Production of Pro-inflammatory Cytokines
Author: Daniel Svensson; Alexandra Aidoukovitch; Emma Anders;
Daniel Jonsson; Daniel Nebel; Bengt-Olof Nilsson

Presented by: Fibe Yulinda Cesa(196070100111002)

 Introduction

Expressing:
1. bone marker protein
2. alkaline phospatase activity
3. mineralized nodule formation

Produce Inflammatory
fibrous cells
cytokines (IL-6; IL-1β)

Source: toothbody.com; inflammatory

enhanced
reaction (tissue
healing
inflamation)

LEGENDS regulatory mechanism periodontitis

AC : alveolar crest fibers poorly understood
H : horizontal fibers
OBL : oblique fibers
PA : periapical fibers
IR : interradicular fibers Source: dental.pitt.edu/
Introduction Secretory Leukocyte
Protease Inhibitor (SLPI)

a potent inhibitor of serine proteases

found in saliva, nasal secretion and expressed by:
• oral
• bronchial epithelial cells
• human HaCaT keratinocytes
translocates from cytoplasm to nucleus and binds to NF-jB binding
sites in the promoter region of the TNF-a and IL-8 (CXCL-8) genes
The secretory form of SLPI has been shown to interact with LPS
and thus inhibit the binding of LPS to its cell surface receptors

The aim :
investigate the hypothesis that “SLPI governs pro-inflammatory cytokine expression in
human PDL cells; determines their sensitivity to LPS and to assess underlying mechanisms
with focus on the NF-jB signaling pathway”
Materials and
Methods

Cells and cell culture Transfection with

PDL Cells from 3 boys 3 girls
12-16 years of age siRNA for SLPI

Quantitative real- Statistics

time RT-PCR Western
Immunocytochemistry Blotting
 Result
Human PDL cells express SLPI
Human PDL cells express SLPI (cont...)
 Result
Knockdown of SLPI by siRNA enhances PDL cell
gene expression of IL-6, MCP-1, and TLRs
Knockdown of SLPI by siRNA enhances PDL cell gene expression of IL-6, MCP-1, and TLRs (cont..)
Result

Knockdown of SLPI enhances

PDL cell expression of MCP-1
protein
 Result
Knockdown of SLPI by siRNA increases the expression
of phosphorylated NF-κB p105 protein in PDL cells
 Discussion

Knockdown negativelly regulates human PDL cell expression of pro-

inflammatory cytokines IL-6 & MCP-1
of SLPI by
siRNA controls PDL cells cyokines expression both transcript and protein
level

• enhanced LPS-induced
• enhanced basal expression of cytokines
• suppresses both stimulated & constitutive PDL cell reproduction
of cytokines
• it acts intracellular in PDL cells
• siRNA for up-regulated IL-6, MCP-1, TLR 2, and TLR 4
expression regulates microbial/endotoxin signalling
• The human PDL cells expressed the SLPI protein but their expression level
was lower than for human epithelial HaCaT cells. There is an observation of a
negative correlation between LPS-induced
• cytokine expression and cellular levels of SLPI : SLPI regulates cytokines
expression in PDL cells

Knockdown of SLPI is associated with modulation of the NF-κB signaling

pathway in human PDL cells, suggesting that SLPI regulates PDL cell production
of pro-inflammatory cytokines through this mechanism. Silencing the SLPI gene
elevated the phosphorylated NF-κB p105 expression, proposing that down-
regulation of SLPI may enhance NF-κB activity via this mechanism.
 Summary

1. SLPI regulates the human PDL cell expression of the pro-

inflammatory cytokines IL-6 and MCP-1 and that effect is
associated with modulation of TLR2 and TLR4 expression and
the NF-κB signaling pathway
2. SLPI represents a novel mechanism that governs the immune cell-
like properties of PDL cells,which may be of importance in the
pathogenesis of periodontitis
 Critical Appraisal

2. The content and methods

are presented properly

3. they didn't mention the

difference between samples
(boys and girls)

Page 827

1. Uncomfortable picture
arrangements

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THANK
Y O U