Journal
MOLECULAR IMMUNOLOGY
Volume 48, Issue 1-3, Pages 356-364Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.molimm.2010.07.004
Keywords
TLR4; Rodent; Mucosa; Complement; Inflammation
Categories
Funding
- NIH of the NCRR [AI061691, P20 RR017686, RR016475]
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Innate immune responses including TLR4 and complement activation are required for mesenteric ischemia/reperfusion (IR)-induced tissue damage We examined the regulation of TLR4 and complement activation in a mouse model of intestinal IR Intestinal IR-induced C3 deposition in a TLR4 dependent manner In addition in wild-type but not TLR4 deficient mice IR significantly increased C3 and Factor B (FB) mRNA expression within the intestine To further examine the role of TLR4 and complement we administered the complement inhibitor CR2-Crry to target local complement activation in wild-type C57BI/10 and TLR4 deficient B10/ScN mice TLR4 deficient mice sustained less damage and inflammation after IR than wild-type mice but administration of CR2-Crry did not further reduce tissue damage In contrast CR2-Crry treatment of wild-type mice was accompanied by a reduction in complement activation and in C3 and FB transcription in response to IR CR2-Crry also significantly decreased intestinal IL-6 and IL-12p40 production in both the wild-type and TLR4 deficient mice These data indicate that TLR4 regulates extrahepatic complement production while complement regulates TLR4-mediated cytokine production during intestinal IR (C) 2010 Elsevier Ltd All rights reserved
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