Induction of apoptosis in murine macrophages by Mycobacterium tuberculosis is reactive oxygen intermediates-independent

Biochem Biophys Res Commun. 1998 Jun 18;247(2):436-42. doi: 10.1006/bbrc.1998.8802.

Abstract

Infection with Mycobacterium tuberculosis induces apoptosis in murine macrophage lines. Resistant macrophages B10R (Bcgr) are more prone to undergo apoptosis than susceptible B10S (Bcgs) macrophages. Apoptosis and inhibition of intracellular growth of the mycobacteria seem to be dependent on the production of nitric oxide, since both can be reverted by aminoguanidine (AMG). Although B10R macrophages produce more superoxide anion than B10S macrophages after infection with M. tuberculosis, reactive oxygen intermediate (ROIs) scavengers did not affect uptake of 3H-uracil incorporation by the mycobacteria nor the induction of apoptosis. These results further suggest that both phenomena are dependent on the production of nitric oxide by the infected macrophages.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology*
  • Cell Line
  • Enzyme Inhibitors / pharmacology
  • Free Radical Scavengers / pharmacology
  • Guanidines / pharmacology
  • Macrophages / cytology*
  • Macrophages / drug effects
  • Macrophages / metabolism*
  • Mice
  • Mycobacterium tuberculosis / growth & development
  • Mycobacterium tuberculosis / pathogenicity*
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitrites / pharmacology
  • Reactive Oxygen Species / metabolism*
  • Superoxides / metabolism
  • Tuberculosis / metabolism
  • Tuberculosis / pathology

Substances

  • Enzyme Inhibitors
  • Free Radical Scavengers
  • Guanidines
  • Nitrites
  • Reactive Oxygen Species
  • Superoxides
  • Nitric Oxide Synthase
  • pimagedine