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*
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Department of Cell Biology and Immunology, Free University, Amsterdam, The Netherlands;
Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195
The host response to Gram-negative LPS is characterized by an
influx of inflammatory cells into host tissues, which is mediated, in
part, by localized production of chemokines. The expression and
function of chemokines in vivo appears to be highly selective, though
the molecular mechanisms responsible are not well understood. All CXC
(IFN-
-inducible protein (IP-10), macrophage inflammatory protein
(MIP)-2, and KC) and CC (JE/monocyte chemoattractant protein (MCP)-1,
MCP-5, MIP-1
, MIP-1
, and RANTES) chemokine genes evaluated were
sensitive to stimulation by LPS in vitro and in vivo. While IL-10
suppressed the expression of all LPS-induced chemokine genes evaluated
in vitro, treatment with IFN- selectively induced IP-10 and MCP-5
mRNAs, but inhibited LPS-induced MIP-2, KC, JE/MCP-1, MIP-1, and
MIP-1 mRNA and/or protein. Like the response to IFN-,
LPS-mediated induction of IP-10 and MCP-5 was Stat1 dependent.
Interestingly, only the IFN--mediated suppression of LPS-induced KC
gene expression was IFN regulatory factor-2 dependent. Treatment of
mice with LPS in vivo also induced high levels of chemokine mRNA in the
liver and lung, with a concomitant increase in circulating protein.
Hepatic expression of MIP-1, MIP-1, RANTES, and MCP-5 mRNAs were
dramatically reduced in Kupffer cell-depleted mice, while IP-10, KC,
MIP-2, and MCP-1 were unaffected or enhanced. These findings indicate
that selective regulation of chemokine expression in vivo may result
from differential response of macrophages to pro- and antiinflammatory
stimuli and to cell type-specific patterns of stimulus sensitivity.
Moreover, the data suggest that individual chemokine genes are
differentially regulated in response to LPS, suggesting unique roles
during the sepsis cascade.
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M. C. Bosco, A. Rapisarda, S. Massazza, G. Melillo, H. Young, and L. Varesio The Tryptophan Catabolite Picolinic Acid Selectively Induces the Chemokines Macrophage Inflammatory Protein-1{alpha} and -1{beta} in Macrophages J. Immunol., March 15, 2000; 164(6): 3283 - 3291. [Abstract] [Full Text] [PDF]
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 Z.-M. Wang, C. Liu, and R. Dziarski Chemokines Are the Main Proinflammatory Mediators in Human Monocytes Activated by Staphylococcus aureus, Peptidoglycan, and Endotoxin J. Biol. Chem., June 30, 2000; 275(27): 20260 - 20267. [Abstract] [Full Text] [PDF]
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E. Trogan, R. P. Choudhury, H. M. Dansky, J. X. Rong, J. L. Breslow, and E. A. Fisher Laser capture microdissection analysis of gene expression in macrophages from atherosclerotic lesions of apolipoprotein E-deficient mice PNAS, February 19, 2002; 99(4): 2234 - 2239. [Abstract] [Full Text] [PDF]
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L. H. K. Lim, B. S. Bochner, and E. M. Wagner Leukocyte recruitment in the airways: an intravital microscopic study of rat tracheal microcirculation Am J Physiol Lung Cell Mol Physiol, May 1, 2002; 282(5): L959 - L967. [Abstract] [Full Text] [PDF]
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