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J. Biol. Chem., Vol. 278, Issue 11, 9496-9502, March 14, 2003
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From the The BCL-2 family member BAX plays a critical role
in regulating apoptosis. Surprisingly, bax-deficient
mice display limited phenotypic abnormalities. Here we investigate the
effect of BAX on infection by the sexually transmitted pathogen,
Chlamydia muridarum (the mouse pneumonitis strain of
Chlamydia trachomatis). Bax
Role of Proapoptotic BAX in Propagation of Chlamydia
muridarum (the Mouse Pneumonitis Strain of Chlamydia
trachomatis) and the Host Inflammatory Response*
§,¶
,, Université Paris 7, Institut Pasteur,
Unité de Biologie Moléculaire du Gène, INSERM U277,
Paris, France, ** Sacred Heart Medical Center, Department of
Laboratory Medicine, Spokane, Washington 99220, Howard Hughes Medical Institute,
Departments of Pathology and Medicine, Harvard Medical School,
Dana-Farber Cancer Institute, Boston, Massachusetts 02115, and the
§§ Department of Microbiology and
Immunology, University of Arkansas for Medical Sciences,
Little Rock, Arkansas 72205
/
cells are relatively resistant to Chlamydia-induced
apoptosis, and fewer bacteria are recovered after two infection cycles
from Bax/ cells than from wild-type cells.
These results suggest that BAX-dependent apoptosis may be
used to initiate a new round of infection, most likely by releasing
Chlamydia-containing apoptotic bodies from infected cells
that could be internalized by neighboring uninfected cells.
Nonetheless, infected Bax/ cells die
through necrosis, which is normally associated with inflammation, more
often than infected wild-type cells. These studies were confirmed in
mice infected intravaginally with C. muridarum; since the
infection disappears more quickly from Bax/
mice than from wild-type mice, secretion of proinflammatory cytokines is increased in Bax/ mice, and large
granulomas are present in the genital tract of Bax/ mice. Taken together, these data
suggest that chlamydia-induced apoptosis via BAX contributes to
bacterial propagation and decreases inflammation. Bax
deficiency results in lower infection and an increased inflammatory
cytokine response associated with more severe pathology.
*
This work was supported by the Institut Pasteur (PTR 60),
INSERM, Université Paris 7, National Institutes of Health Grant AI054624, and the Bates-Wheeler Foundations, Arkansas Children's Hospital Research Institute.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Institut Jacques
Monod, Universite Paris 7, 2 place Jussieu, Tour 43, 75251 Paris cedex
05, France. Fax: 33-1-44275265; E-mail: ojcius@noos.fr.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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