Source:http://linkedlifedata.com/resource/pubmed/id/17374847
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2007-7-19
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pubmed:abstractText |
Chlamydia pneumoniae, an intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule myeloid differentiation factor-88 (MyD88) play a critical role in inducing immunity against this microorganism and are crucial for survival. To explore the influence of MyD88 on induction of immune responses in vivo on a genome-wide level, wildtype (WT) or MyD88(-/-) mice were infected with C. pneumoniae on anesthesia, and the pulmonary transcriptome was analyzed 3 days later by microarrays. We found that the infection caused pulmonary cellular infiltration in WT but not MyD88(-/-) mice. Furthermore, it induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88(-/-) mice. This cluster contains primarily genes encoding for chemokines and cytokines like MIP-1alpha, MIP-2, MIP-1gamma, MCP-1, TNF, and KC and other immune effector molecules like immunoresponsive gene-1 and TLR2. Arginase was highly induced after C. pneumoniae infection and was MyD88 dependent. Genes induced by interferons were abundant in a cluster of 102 genes that were only partially MyD88 dependent. Also, lcn2 (lipocalin-2) and timp1 were represented within this cluster. Interestingly, a set of 37 genes including sprr1a was induced more strongly in MyD88(-/-) mice, and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome on infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses and identified MyD88-independent genes involved in cellular replication.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1531-2267
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
18
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
134-45
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pubmed:meshHeading |
pubmed-meshheading:17374847-Animals,
pubmed-meshheading:17374847-Base Sequence,
pubmed-meshheading:17374847-Blotting, Northern,
pubmed-meshheading:17374847-Chlamydia Infections,
pubmed-meshheading:17374847-Chlamydophila pneumoniae,
pubmed-meshheading:17374847-DNA Primers,
pubmed-meshheading:17374847-Lung,
pubmed-meshheading:17374847-Mice,
pubmed-meshheading:17374847-Mice, Inbred C57BL,
pubmed-meshheading:17374847-Mice, Knockout,
pubmed-meshheading:17374847-Myeloid Differentiation Factor 88,
pubmed-meshheading:17374847-RNA, Messenger,
pubmed-meshheading:17374847-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2007
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pubmed:articleTitle |
MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae.
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pubmed:affiliation |
Institute of Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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