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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2009-8-6
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pubmed:abstractText |
The resistance of epithelial cells infected with Chlamydophila pneumoniae for apoptosis has been attributed to the induced expression and increased stability of anti-apoptotic proteins called inhibitor of apoptosis proteins (IAPs). The significance of cellular inhibitor of apoptosis protein-1 (cIAP-1) in C. pneumoniae pulmonary infection and innate immune response was investigated in cIAP-1 knockout (KO) mice using a novel non-invasive intra-tracheal infection method. In contrast to wildtype, cIAP-1 knockout mice failed to clear the infection from their lungs. Wildtype mice responded to infection with a strong inflammatory response in the lung. In contrast, the recruitment of macrophages was reduced in cIAP-1 KO mice compared to wildtype mice. The concentration of Interferon gamma (IFN-gamma) was increased whereas that of Tumor Necrosis Factor (TNF-alpha) was reduced in the lungs of infected cIAP-1 KO mice compared to infected wildtype mice. Ex vivo experiments on mouse peritoneal macrophages and splenocytes revealed that cIAP-1 is required for innate immune responses of these cells. Our findings thus suggest a new immunoregulatory role of cIAP-1 in the course of bacterial infection.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:issn |
1932-6203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
e6519
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pubmed:meshHeading |
pubmed-meshheading:19657383-Animals,
pubmed-meshheading:19657383-Chlamydia Infections,
pubmed-meshheading:19657383-Chlamydophila pneumoniae,
pubmed-meshheading:19657383-Immunity, Innate,
pubmed-meshheading:19657383-Inhibitor of Apoptosis Proteins,
pubmed-meshheading:19657383-Interferon-gamma,
pubmed-meshheading:19657383-Lung Diseases,
pubmed-meshheading:19657383-Macrophages, Peritoneal,
pubmed-meshheading:19657383-Mice,
pubmed-meshheading:19657383-Mice, Knockout,
pubmed-meshheading:19657383-Nitric Oxide,
pubmed-meshheading:19657383-Spleen,
pubmed-meshheading:19657383-Tumor Necrosis Factor-alpha
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pubmed:year |
2009
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pubmed:articleTitle |
cIAP-1 controls innate immunity to C. pneumoniae pulmonary infection.
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pubmed:affiliation |
Department of Molecular Biology, Max Planck Institute for Infection Biology, Charitéplatz 1, Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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