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*
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Immunobiology Research Group, Gesellschaft für Biotechnologische Forschung, Braunschweig, Germany; and
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo, Japan
A family of Toll-like receptor (TLR) mediates the cellular response
to bacterial cell wall components; murine TLR2 and TLR4 recognize
mycoplasmal lipopeptides (macrophage-activating lipopeptides, 2 kDa
(MALP-2)) and LPS, respectively. Costimulation of mouse peritoneal
macrophages with MALP-2 and LPS results in a marked increase in TNF-
production, showing the synergy between TLR2- and TLR4-mediated
signaling pathways. Macrophages pretreated with LPS show
hyporesponsiveness to the second LPS stimulation, termed LPS tolerance.
The LPS tolerance has recently been shown to be primarily due to the
down-regulation of surface expression of the TLR4-MD2 complex. When
macrophages were treated with MALP-2, the cells showed
hyporesponsiveness to the second MALP-2 stimulation, like LPS
tolerance. Furthermore, macrophages pretreated with MALP-2 showed
reduced production of TNF- in response to LPS. LPS-induced
activation of both NF-
B and c-Jun NH2-terminal kinase
was severely impaired in MALP-2-pretreated cells. However,
MALP-2-pretreated macrophages did not show any reduction in surface
expression of the TLR4-MD2 complex. These findings indicate that
LPS-induced LPS tolerance mainly occurs through the down-regulation of
surface expression of the TLR4-MD2 complex; in contrast, MALP-2-induced
LPS tolerance is due to modulation of the downstream cytoplasmic
signaling pathways.
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