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Dendritic cell activation in response to ischemia-reperfusion injury of the small intestine.

Authors: Hagiwara, S  Iwasaka, H  Hasegawa, A  Asai, N  Uchida, T  Noguchi, T 
Citation: Hagiwara S, etal., Surg Today. 2010;40(2):137-45. Epub 2010 Jan 28.
Pubmed: (View Article at PubMed) PMID:20107953
DOI: Full-text: DOI:10.1007/s00595-009-4033-6

PURPOSE: Recent studies have increased our understanding of the important role that the immune system plays in ischemia-reperfusion (I/R) injury. Although dendritic cells (DCs) are important regulators of intestinal immunity, their role in the response to intestinal I/R injury is not well understood. The aim of this study was to determine whether I/R injury affects DC infiltration into the intestinal barrier. METHODS: Wistar rats were subjected to I/R injury or a sham operation. Dendritic cells were visualized by immunohistochemistry, and after 12 h of reperfusion protein levels for nucleotide-binding oligomerization domain protein 2 (NOD2), high-mobility group box 1 (HMGB1), and Toll-like receptor 4 (TLR4) were assayed by Western blotting. RESULTS: The number of DCs increased at the small intestine barrier in response to intestinal I/R. A Western blot analysis of small intestinal tissue revealed that levels of NOD2, HMGB1, and TLR4 protein increased in rats subjected to I/R injury in comparison to control rats. CONCLUSIONS: These results suggest that intestinal I/R increases the infiltration of DCs into the small intestine, thus potentially involving the upregulation of NOD2, HMGB1, and TLR4. Therefore, intestinal I/R might activate DCs through NOD2 and HMGB1.

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RGD Object Information
RGD ID: 5131440
Created: 2011-04-27
Species: All species
Last Modified: 2011-04-27
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.