Induction of murine macrophage TNF-α synthesis byMycobacterium aviumis modulated through complement-dependent interaction via complement receptors 3 and 4 in relation toM. aviumglycopeptidolipid
Autor: | Joel N. Maslow, Vida R. Irani |
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Rok vydání: | 2005 |
Předmět: |
Mutant
Virulence Complement receptor Microbiology Cell Line Mice Genetics Animals Humans Macrophage Molecular Biology Mycobacterium avium-intracellulare Infection biology Tumor Necrosis Factor-alpha Macrophages Glycopeptides Complement C4 Complement C3 Mycobacterium avium Complex biology.organism_classification Molecular biology Receptors Complement Biochemistry iC3b Tumor necrosis factor alpha Glycolipids Signal transduction Mycobacterium |
Zdroj: | FEMS Microbiology Letters. 246:221-228 |
ISSN: | 1574-6968 0378-1097 |
DOI: | 10.1016/j.femsle.2005.04.008 |
Popis: | 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. |
Databáze: | OpenAIRE |
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