Affiliation:
1. Department
of Periodontics, University of Washington, Seattle, Washington
98195
Abstract
ABSTRACT
E.
coli
lipopolysaccharide (LPS) induces cytokine and adhesion
molecule expression via the toll-like receptor 4 (TLR4) signaling
complex in human endothelial cells. In the present study, we
investigated the mechanism by which
Porphyromonas gingivalis
LPS antagonizes
E. coli
LPS-dependent activation of human
endothelial cells.
P. gingivalis
LPS at 1 μg/ml
inhibited both
E. coli
LPS (10 ng/ml) and
Mycobacterium
tuberculosis
heat shock protein (HSP) 60.1 (10 μg/ml)
stimulation of E-selectin mRNA expression in human umbilical vein
endothelial cells (HUVEC) without inhibiting interleukin-1 beta
(IL-1β) stimulation.
P. gingivalis
LPS (1μ
g/ml) also blocked both
E. coli
LPS-dependent and
M. tuberculosis
HSP60.1-dependent but not
IL-1β-dependent activation of NF-κB in human
microvascular endothelial (HMEC-1) cells, consistent with antagonism
occurring upstream from the TLR/IL-1 receptor adaptor protein, MyD88.
Surprisingly,
P. gingivalis
LPS weakly but significantly
activated NF-κB in HMEC-1 cells in the absence of
E.
coli
LPS, and the
P. gingivalis
LPS-dependent agonism was
blocked by transient expression of a dominant negative murine TLR4.
Pretreatment of HUVECs with
P. gingivalis
LPS did not
influence the ability of
E. coli
LPS to stimulate E-selectin
mRNA expression. Taken together, these data provide the first evidence
that
P. gingivalis
LPS-dependent antagonism of
E.
coli
LPS in human endothelial cells likely involves the ability of
P. gingivalis
LPS to directly compete with
E. coli
LPS at the TLR4 signaling
complex.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
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