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Departments of
*
Microbiology and
Oral Biology, University of Alabama, Birmingham, AL 35294; and
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814
Exposure of mononuclear phagocytes to enterobacterial LPS induces a
state of transient hyporesponsiveness to subsequent LPS exposure,
termed endotoxin tolerance. In the present study, LPS derived from the
oral periodontal pathogen, Porphyromonas gingivalis, was
compared with that derived from the enterobacterium, Escherichia
coli, for the ability to induce endotoxin tolerance.
Pretreatment of the human macrophage cell line, THP-1, with E.
coli LPS resulted in a severe reduction in the levels of
IL-1
, IL-6, and TNF-
upon secondary stimulation. In contrast,
pretreatment of THP-1 cells with P. gingivalis LPS
resulted in a mitigation of IL-1, but not IL-6 and TNF-
production upon subsequent exposure to P. gingivalis
LPS: primary or secondary stimulation with 
100 ng/ml P.
gingivalis LPS resulted in comparable levels of IL-6 and
TNF-, while stimulation of THP-1 cells with 
1 µg/ml P.
gingivalis LPS induced a significant enhancement in IL-6 and
TNF- levels upon secondary exposure. To identify possible mechanisms
for these differences, changes in the expression of molecules involved
in the LPS-signaling pathway were assessed. Pretreatment of THP-1 cells
with E. coli LPS resulted in a significant reduction in
surface Toll-like receptor 4 (TLR4) expression and an inability to
degrade I-
B- or I-B- proteins upon secondary
stimulation. In contrast, pretreatment of THP-1 cells with P.
gingivalis LPS resulted in a significant enhancement of both
CD14 and TLR2, while maintaining the ability to degrade I-B-
only upon secondary stimulation. Thus, E. coli and
P. gingivalis LPS differentially affect CD14 and TLR
expression as well as secondary LPS-associated
responses.
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