TLR9 is dispensable for intestinal ischemia/reperfusion-induced tissue damage

dc.citation.epage135en_US
dc.citation.issue2en_US
dc.citation.jtitleAmerican Journal of Clinical and Experimental Immunologyen_US
dc.citation.spage124en_US
dc.citation.volume1en_US
dc.contributor.authorSlone, Emily Archer
dc.contributor.authorPope, Michael R.
dc.contributor.authorRoth, Mary R.
dc.contributor.authorWelti, Ruth
dc.contributor.authorFleming, Sherry D.
dc.contributor.authoreidmpopeen_US
dc.contributor.authoreidmrrothen_US
dc.contributor.authoreidweltien_US
dc.contributor.authoreidsdfleminen_US
dc.date.accessioned2013-10-03T20:53:59Z
dc.date.available2013-10-03T20:53:59Z
dc.date.issued2013-10-03
dc.date.published2012en_US
dc.description.abstractThe mortality rate due to intestinal ischemia/reperfusion (IR) remains at 60-80%. As toll-like receptor (TLR) 4 has been shown to be critical for IR injury in several organs, including the intestine, and TLR9 is necessary for IR-induced damage of the liver, we investigated the hypothesis that TLR9 is involved in intestinal IR-induced damage. Wildtype (C57Bl/6) and TLR9[superscript -/-] mice were subjected to intestinal IR or Sham treatment. Several markers of damage and inflammation were assessed, including mucosal injury, eicosanoid production, cytokine secretion and complement deposition. Although IR-induced injury was not altered, PGE[subscript 2] production was decreased in TLR9[superscript -/-] mice. Attenuated PGE[subscript 2] production was not due to differences in percentage of lipids or COX-2 transcription. The data indicate that TLR9 is not required for IR-induced injury or inflammation of the intestine.en_US
dc.identifier.urihttp://hdl.handle.net/2097/16603
dc.language.isoen_USen_US
dc.relation.urihttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509382/en_US
dc.subjectMouseen_US
dc.subjectIntestineen_US
dc.subjectComplementen_US
dc.subjectTLRsen_US
dc.subjectIschemiaen_US
dc.titleTLR9 is dispensable for intestinal ischemia/reperfusion-induced tissue damageen_US
dc.typeArticle (publisher version)en_US

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