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J. Biol. Chem., Vol. 277, Issue 39, 36068-36075, September 27, 2002
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From the Department of Academic Surgery, National University of
Ireland, Cork University Hospital, Cork, Ireland
Tolerance to bacterial cell wall components
including lipopolysaccharide (LPS) may represent an essential
regulatory mechanism during bacterial infection. Two members of the
Toll-like receptor (TLR) family, TLR2 and TLR4, recognize the specific
pattern of bacterial cell wall components. TLR4 has been found to be
responsible for LPS tolerance. However, the role of TLR2 in bacterial
lipoprotein (BLP) tolerance and LPS tolerance is unclear. Pretreatment
of human THP-1 monocytic cells with a synthetic bacterial lipopeptide induced tolerance to a second BLP challenge with diminished tumor necrosis factor-
Induction of Bacterial Lipoprotein Tolerance Is Associated with
Suppression of Toll-like Receptor 2 Expression*
§,,
and interleukin-6 production, termed BLP tolerance. Furthermore, BLP-tolerized THP-1 cells no longer responded to LPS
stimulation, indicating a cross-tolerance to LPS. Induction of BLP
tolerance was CD14-independent, as THP-1 cells that lack membrane-bound
CD14 developed tolerance both in serum-free conditions and in the
presence of a specific CD14 blocking monoclonal antibody (MEM-18).
Pre-exposure of THP-1 cells to BLP suppressed mitogen-activated protein
kinase phosphorylation and nuclear factor-
B activation in response
to subsequent BLP and LPS stimulation, which is comparable with that
found in LPS-tolerized cells, indicating that BLP tolerance and LPS
tolerance may share similar intracellular pathways. However, BLP
strongly enhanced TLR2 expression in non-tolerized THP-1 cells, whereas
LPS stimulation had no effect. Furthermore, a specific TLR2 blocking
monoclonal antibody (2392) attenuated BLP-induced, but not LPS-induced,
tumor necrosis factor- and interleukin-6 production, indicating BLP
rather than LPS as a ligand for TLR2 engagement and activation. More
importantly, pretreatment of THP-1 cells with BLP strongly inhibited
TLR2 activation in response to subsequent BLP stimulation. In contrast,
LPS tolerance did not prevent BLP-induced TLR2 overexpression. These
results demonstrate that BLP tolerance develops through down-regulation
of TLR2 expression.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Both authors contributed equally to this work.
§
To whom correspondence should be addressed: Dept. of Academic
Surgery, National University of Ireland, Cork University Hospital, Wilton, Cork, Ireland. Tel.: 353-21-4901275; Fax: 353-21-4901240; E-mail: jh.wang@ucc.ie.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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