Source:http://linkedlifedata.com/resource/pubmed/id/12509420
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2003-3-10
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pubmed:abstractText |
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(-/-) 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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bax protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
14
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pubmed:volume |
278
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
9496-502
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12509420-Animals,
pubmed-meshheading:12509420-Apoptosis,
pubmed-meshheading:12509420-Chlamydia Infections,
pubmed-meshheading:12509420-Chlamydia muridarum,
pubmed-meshheading:12509420-Female,
pubmed-meshheading:12509420-Granuloma,
pubmed-meshheading:12509420-Inflammation,
pubmed-meshheading:12509420-Mice,
pubmed-meshheading:12509420-Mice, Inbred C57BL,
pubmed-meshheading:12509420-Mice, Transgenic,
pubmed-meshheading:12509420-Necrosis,
pubmed-meshheading:12509420-Proto-Oncogene Proteins,
pubmed-meshheading:12509420-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:12509420-Time Factors,
pubmed-meshheading:12509420-bcl-2-Associated X Protein
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pubmed:year |
2003
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pubmed:articleTitle |
Role of proapoptotic BAX in propagation of Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) and the host inflammatory response.
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pubmed:affiliation |
Université Paris 7, Institut Pasteur, Unité de Biologie Moléculaire du Gène, INSERM U277, Paris, France.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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