Late acquisition of hyporesponsiveness to lipopolysaccharide by Mycobacterium avium-infected human macrophages in producing tumor necrosis factor-alpha but not interleukin-1 beta and -6

J Infect Dis. 1996 Apr;173(4):1030-4. doi: 10.1093/infdis/173.4.1030.

Abstract

To investigate whether infection with Mycobacterium avium modifies the cytokine response of human macrophages (Mphi) to lipopolysaccharide (LPS), the release of interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha was determined in infected and uninfected Mphi, unstimulated or stimulated with LPS. In unstimulated Mphi, the release of IL-1 beta and IL-6 increased with the progress of infection while that of TNF-alpha progressively decreased. When Mphi were stimulated with LPS, IL-1 beta and IL-6 levels were always higher in infected than in uninfected cells, but levels of TNF-alpha significantly decreased in infected Mphi. A similar trend was obtained for TNF-alpha mRNA expression. Altogether, these results indicate that infected Mphi react to LPS stimulus with enhanced levels of IL-1 beta and IL-6 but are unable to restore the production of TNF-alpha impaired by the growth of the intracellular mycobacteria.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Gene Expression
  • Humans
  • Interleukin-1 / biosynthesis*
  • Interleukin-6 / biosynthesis*
  • Lipopolysaccharides / immunology*
  • Macrophage Activation
  • Macrophages / microbiology
  • Macrophages / physiology*
  • Mycobacterium avium Complex / growth & development
  • Mycobacterium avium Complex / immunology*
  • Mycobacterium avium-intracellulare Infection / immunology*
  • RNA, Messenger / genetics
  • Time Factors
  • Tumor Necrosis Factor-alpha / biosynthesis*

Substances

  • Interleukin-1
  • Interleukin-6
  • Lipopolysaccharides
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha