Fas ligand-induced apoptosis of infected human macrophages reduces the viability of intracellular Mycobacterium tuberculosis.

Details

Serval ID
serval:BIB_2D657CBEB8A8
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Fas ligand-induced apoptosis of infected human macrophages reduces the viability of intracellular Mycobacterium tuberculosis.
Journal
Journal of immunology
Author(s)
Oddo M., Renno T., Attinger A., Bakker T., MacDonald H.R., Meylan P.R.
ISSN
0022-1767
Publication state
Published
Issued date
1998
Peer-reviewed
Oui
Volume
160
Number
11
Pages
5448-5454
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Mycobacterium tuberculosis-specific cytolytic activity is mediated mostly by CD4+CTL in humans. CD4+CTL kill infected target cells by inducing Fas (APO-1/CD95)-mediated apoptosis. We have examined the effect of Fas ligand (FasL)-induced apoptosis of human macrophages infected in vitro with M. tuberculosis on the viability of the intracellular bacilli. Human macrophages expressed Fas and underwent apoptosis after incubation with soluble recombinant FasL. In macrophages infected either with an attenuated (H37Ra) or with a virulent (H37Rv) strain of M. tuberculosis, the apoptotic death of macrophages was associated with a substantial reduction in bacillary viability. TNF-induced apoptosis of infected macrophages was coupled with a similar reduction in mycobacterial viability, while the induction of nonapoptotic complement-induced cell death had no effect on bacterial viable counts. Infected macrophages also showed a reduced susceptibility to FasL-induced apoptosis correlating with a reduced level of Fas expression. These data suggest that apoptosis of infected macrophages induced through receptors of the TNF family could be an immune effector mechanism not only depriving mycobacteria from their growth environment but also reducing viable bacterial counts by an unknown mechanism. On the other hand, interference by M. tuberculosis with the FasL system might represent an escape mechanism of the bacteria attempting to evade the effect of apoptosis.
Keywords
Antigens, CD95/biosynthesis, Antigens, CD95/physiology, Apoptosis/immunology, Cell Death/immunology, Colony Count, Microbial, Fas Ligand Protein, Humans, Immunity, Innate, Intracellular Fluid/immunology, Intracellular Fluid/microbiology, Ligands, Macrophages/cytology, Macrophages/immunology, Membrane Glycoproteins/biosynthesis, Membrane Glycoproteins/physiology, Mycobacterium tuberculosis/growth &amp, development, Mycobacterium tuberculosis/immunology
Pubmed
Web of science
Create date
25/01/2008 14:33
Last modification date
20/08/2019 13:12
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