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Am J Clin Exp Immunol 2012;1(2):124-135
Review Article
TLR9 is dispensable for intestinal ischemia/reperfusion-induced tissue
damage
Emily Archer Slone, Michael R Pope, Mary Roth, Ruth Welti, Sherry D Fleming
Division of Biology, 18 Ackert Hall, Kansas State University, Manhattan, KS 66506, USA
Received August 20, 2012; Accepted September 17, 2012; Epub September 27, 2012; Published November 30, 2012
Abstract: The 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-/- 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, PGE2 production was decreased in TLR9-
/- mice. Attenuated PGE2 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. (AJCEI1208003).
Keywords: Mouse, intestine, complement, TLRs, ischemia
Address all correspondence to:
Dr. Sherry D Fleming
Division of Biology, 18 Ackert Hall
Kansas State University, Manhattan, KS 66506, USA.
Tel: 785-532-6130; Fax: 785-532-6653
E-mail: sdflemin@ksu.edu
Review Article
TLR9 is dispensable for intestinal ischemia/reperfusion-induced tissue
damage
Emily Archer Slone, Michael R Pope, Mary Roth, Ruth Welti, Sherry D Fleming
Division of Biology, 18 Ackert Hall, Kansas State University, Manhattan, KS 66506, USA
Received August 20, 2012; Accepted September 17, 2012; Epub September 27, 2012; Published November 30, 2012
Abstract: The 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-/- 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, PGE2 production was decreased in TLR9-
/- mice. Attenuated PGE2 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. (AJCEI1208003).
Keywords: Mouse, intestine, complement, TLRs, ischemia
Address all correspondence to:
Dr. Sherry D Fleming
Division of Biology, 18 Ackert Hall
Kansas State University, Manhattan, KS 66506, USA.
Tel: 785-532-6130; Fax: 785-532-6653
E-mail: sdflemin@ksu.edu
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