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Infection and Immunity, December 2005, p. 8136-8143, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8136-8143.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Regulation of Cellular Caveolin-1 Protein Expression in Murine Macrophages by Microbial Products

Mei G. Lei,* Xiaoyu Tan, Nilofer Qureshi, and David C. Morrison

Department of Basic Medical Science and Shock/Trauma Research Center, University of Missouri at Kansas City, School of Medicine, Kansas City, Missouri 64108

Received 20 July 2005/ Accepted 31 August 2005

Previously, we reported that expression of caveolin-1 in elicited peritoneal mouse macrophages was up-regulated by remarkably low (1.0-pg/ml) concentrations of Escherichia coli O111 lipopolysaccharide (LPS). Here we report that increases in caveolin-1 expression are manifested by different types of LPS, LPS-mimetic taxol, and heat-killed E. coli and to a much lesser extent by zymosan, polysaccharide-peptidoglycan, and heat-killed Staphylococcus aureus. Rhodobacter sphaeroides lipid A (RsDPLA) could not induce caveolin-1 expression in macrophages. Interestingly, polymyxin B (5 µg/ml) and RsDPLA show only a limited capacity to inhibit LPS-induced caveolin-1 expression. These findings suggest that expression of caveolin-1 in response to LPS may only partially be dependent upon lipid A. Recombinant tumor necrosis factor alpha marginally induces caveolin-1, suggesting that the ability of LPS to regulate caveolin-1 is not mediated primarily through an autocrine/paracrine mechanism involving this cytokine. Under conditions in which cellular levels of caveolin-1 are profoundly induced, no significant changes in TLR4 expression are observed. Of interest, caveolin-1 appears to localize to two cellular compartments, one associated with lipid rafts and a second associated with TLR4. Gamma interferon treatment inhibits the induction of caveolin-1 by LPS in macrophages. Inhibition of the p38 kinase-dependent pathway, but not the extracellular signal-regulated kinase pathway, effectively reduced the ability of LPS to mediate caveolin-1 up-regulation. Lactacystin, a potent inhibitor of the proteasome pathway, significantly modulates LPS-independent caveolin-1 expression, and lactacystin inhibits LPS-triggered caveolin-1 responses. These studies suggest that caveolin-1 up-regulation in response to LPS is likely to be proteasome dependent and triggered through the p38 kinase pathway.

* Corresponding author. Present address: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Slot 511, 4301 W. Markham St., Little Rock, AR 72205. Phone: (501) 526-7937. Fax: (501) 686-5359. E-mail: mglei{at}uams.edu.

Editor: D. L. Burns

Infection and Immunity, December 2005, p. 8136-8143, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8136-8143.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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