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*
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115;
Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; and
Division of Molecular Medicine, North Shore University Hospital, Manhasset, NY 11030
Overproduction of inflammatory mediators by macrophages in response
to Gram-negative LPS has been implicated in septic shock. Recent
reports indicate that three membrane-associated proteins, CD14,
CD11b/CD18, and Toll-like receptor (TLR) 4, may serve as LPS
recognition and/or signaling receptors in murine macrophages.
Therefore, the relative contribution of these proteins in the induction
of cyclooxygenase 2 (COX-2), IL-12 p35, IL-12 p40, TNF-
,
IFN-inducible protein (IP)-10, and IFN consensus sequence binding
protein (ICSBP) genes in response to LPS or the LPS-mimetic, Taxol, was
examined using macrophages derived from mice deficient for these
membrane-associated proteins. The panel of genes selected reflects
diverse macrophage effector functions that contribute to the
pathogenesis of septic shock. Induction of the entire panel of genes in
response to low concentrations of LPS or Taxol requires the
participation of both CD14 and TLR4, whereas high concentrations of LPS
or Taxol elicit the expression of a subset of LPS-inducible genes in
the absence of CD14. In contrast, for optimal induction of COX-2, IL-12
p35, and IL-12 p40 genes by low concentrations of LPS or by all
concentrations of Taxol, CD11b/CD18 was also required. Mitigated
induction of COX-2, IL-12 p35, and IL-12 p40 gene expression by
CD11b/CD18-deficient macrophages correlated with a marked inhibition of
NF-
B nuclear translocation and mitogen-activated protein kinase
(MAPK) activation in response to Taxol and of NF-B nuclear
translocation in response to LPS. These findings suggest that for
expression of a full repertoire of LPS-/Taxol-inducible genes, CD14,
TLR4, and CD11b/CD18 must be coordinately engaged to deliver optimal
signaling to the macrophage.
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