Source:http://linkedlifedata.com/resource/pubmed/id/21056969
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-1-19
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pubmed:abstractText |
Ischaemia-reperfusion-induced intestinal injury requires both Toll-like receptor 4 (TLR4) signalling through myeloid differentiation primary response gene (88) (MyD88) and complement activation. As a common Gram-negative intestinal pathogen, Helicobacter hepaticus signals through TLR4 and upregulates the complement inhibitor, decay accelerating factor (DAF; CD55). Since ischaemia-reperfusion (IR) injury is complement dependent, we hypothesized that Helicobacter infection may alter IR-induced intestinal damage. Infection increased DAF transcription and subsequently decreased complement activation in response to IR without altering intestinal damage in wild-type mice. Ischaemia-reperfusion induced similar levels of DAF mRNA expression in uninfected wild-type,?MyD88(-/-) or TIR-domain-containing adaptor-inducing interferon-? (Trif)-deficient mice. However, during infection, IR-induced DAF transcription was significantly attenuated in Trif-deficient mice. Likewise, IR-induced intestinal damage, complement component 3 deposition and prostaglandin E(2) production were attenuated in Helicobacter-infected, Trif-deficient but not?MyD88(-/-) mice. While infection attenuated IR-induced cytokine production in wild-type and?MyD88(-/-) mice, there was no further decrease in Trif-deficient mice. These data indicate distinct roles for MyD88 and Trif in IR-induced inflammation and suggest that chronic, undetected infections, such as Helicobacter, alter the use of the adaptor proteins to induce damage.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/AI061691,
http://linkedlifedata.com/resource/pubmed/grant/P20 RR017686,
http://linkedlifedata.com/resource/pubmed/grant/P20 RR017686-09,
http://linkedlifedata.com/resource/pubmed/grant/R01 AI061691-04,
http://linkedlifedata.com/resource/pubmed/grant/RR016475
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular...,
http://linkedlifedata.com/resource/pubmed/chemical/Myd88 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Myeloid Differentiation Factor 88,
http://linkedlifedata.com/resource/pubmed/chemical/TICAM-1 protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1469-445X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
104-13
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pubmed:dateRevised |
2011-9-26
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pubmed:meshHeading |
pubmed-meshheading:21056969-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:21056969-Animals,
pubmed-meshheading:21056969-Helicobacter Infections,
pubmed-meshheading:21056969-Intestinal Diseases,
pubmed-meshheading:21056969-Mice,
pubmed-meshheading:21056969-Mice, Inbred C57BL,
pubmed-meshheading:21056969-Mice, Knockout,
pubmed-meshheading:21056969-Myeloid Differentiation Factor 88,
pubmed-meshheading:21056969-Reperfusion Injury,
pubmed-meshheading:21056969-Signal Transduction
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pubmed:year |
2011
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pubmed:articleTitle |
Helicobacter infection alters MyD88 and Trif signalling in response to intestinal ischaemia-reperfusion.
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pubmed:affiliation |
Kansas State University, Division of Biology, Manhattan, KS 66506, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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