Previous Article | Next Article ![]()
Infect. Immun., Oct 1997, 4075-4081, Vol 65, No. 10
J Barsig and SH Kaufmann
Various pathogenic bacteria with the capacity to live within eukaryotic
cells activate an apoptotic program in infected host cells. Induction of
apoptosis by Listeria monocytogenes in murine dendritic cells and
hepatocytes has been described. Here we address the questions of whether
and how the pathogen kills macrophages, its most important habitat.
Employing several complementary techniques aimed at discriminating between
apoptosis and necrosis, we show that murine bone marrow-derived macrophages
(BMM) undergo delayed necrosis but not apoptosis when infected with
listeriolysin (Hly)-producing L. monocytogenes. This pathogen failed to
elicit apoptotic morphology, DNA fragmentation, and surface annexin V
binding of macrophages, in contrast to Shigella flexneri infection or
gliotoxin treatment, which were used as positive controls. Furthermore,
macrophages infected with L. monocytogenes released lower quantities of
interleukin-1beta (IL- 1beta) than did Shigella flexneri-infected ones,
indicating diminished or even absent activation of IL-1-converting enzyme
in macrophages harboring L. monocytogenes. We conclude that murine BMM die
by necrosis after several hours of cytoplasmic replication of L.
monocytogenes. The pathogen may benefit from this feature by the
possibility of taking advantage of cells of "pseudo-healthy" appearance,
thus avoiding rapid elimination by other phagocytes.
Copyright © 1997, American Society for Microbiology
The mechanism of cell death in Listeria monocytogenes-infected murine macrophages is distinct from apoptosis
Department of Immunology, University of Ulm, Germany.
This article has been cited by other articles:
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|