Induction of murine macrophage TNF-α synthesis by Mycobacterium avium is modulated through complement-dependent interaction via complement receptors 3 and 4 in relation to M. avium glycopeptidolipid

Vida R. Irani, Joel N. Maslow

Research output: Contribution to journalArticlepeer-review

Abstract

We studied whether complement receptor (CR) mediated Mycobacterium avium interaction modulated macrophage TNF-α expression. Compared to control conditions, infections performed with C3-depletion yielded significantly higher TNF-α levels. Blockage of the CR4 iC3b site yielded increases in TNF-α 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-α only for SmT and ssGPL-deficient strains. Thus, complement-mediated binding of M. avium to CR3 and CR4 was shown to modulate TNF-α expression. The differential activation of morphotypic and isogenic variants of a single strain provides an excellent model system to delineate signaling pathways.

Original languageEnglish (US)
Pages (from-to)221-228
Number of pages8
JournalFEMS Microbiology Letters
Volume246
Issue number2
DOIs
StatePublished - May 15 2005

Keywords

  • Complement receptor
  • GPL
  • Macrophage
  • Mycobacterium avium
  • Serum proteins
  • TNF-α

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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