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.
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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