Journal
FEMS MICROBIOLOGY LETTERS
Volume 246, Issue 2, Pages 221-228Publisher
WILEY-BLACKWELL
DOI: 10.1016/j.femsle.2005.04.008
Keywords
Mycobacterium avium; GPL; TNF-alpha; macrophage; complement receptor; serum proteins
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Funding
- NIAID NIH HHS [P30-AI-045008-06, 5-UO1-AI32783] Funding Source: Medline
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We studied whether complement receptor (CR) mediated Mycobacterium avium interaction modulated macrophage TNF-alpha expression. Compared to control conditions, infections performed with C3-depletion yielded significantly higher TNF-alpha levels. Blockage of the CR4 iC3b site yielded increases in TNF-alpha for all morphotypic variants of a virulent serovar-8 strain (smooth transparent (SmT), smooth opaque (SmO), serovar-specific glycopeptidolipid (ssGPL) deficient knockout mutant) whereas CR3 blockage increased TNF-alpha only for SmT and ssGPL-deficient strains. Thus, complement-mediated binding of M. avium to CR3 and CR4 was shown to modulate TNF-alpha expression. The differential activation of morphotypic and isogenic variants of a single strain provides an excellent model system to delineate signaling pathways. (c) 2005 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.
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