As a central innate immune regulator, the complement system is activated Poliumoside during intestinal IR and contributes substantially to IR induced inflammation, organ damage and failure. Preventing complement activation has been proven to be beneficial to organ function after IR in general and intestinal IR more specifically. Central in the activation of complement is the formation of C3a, an anaphylatoxin with the ability to attract inflammatory cells into the reperfused ischemic tissue. In our model no deposition of activated C3 in reperfused jejunum was detected, using immunohistochemical and Western blot analysis. Interestingly, our results do however suggest C3 gene Clopidogrel hydrogen sulfate expression in healthy jejunum tissue as well as an increased synthesis of C3 in response to IR. The lack of activated complement components as well as a clear increase in local C3 mRNA expression levels may illustrate the intestines response aimed at protection and preservation. The ability of small intestinal epithelial cells to express biological mediators such as C3 in response to IR was to be expected since previous work demonstrated C3 gene expression in inflamed small intestine. To the best of our knowledge, however, these are the first results that demonstrate C3 mRNA expression in the healthy jejunum. Further analysis will have to elucidate whether increased expression of immune regulatory proteins is directed at preventing gut barrier bacterial translocation. However, when faced with massive intestinal barrier failure, increased expression of immune regulatory proteins able to prevent gut barrier bacterial translocation might be exceedingly useful. The recently discovered molecular mechanism that recognizes and responds to excessive cell death consisting of SAP130 and the macrophage inducible C-type lectin fits in our observations. The loss of excessive numbers of dead cells into the gut lumen prevents SAP130 released by the dead cells to reach tissue macrophages thus largely preventing the production of inflammatory cytokines driving rapid neutrophil infiltration. Similarly activation of complement by dead cells is prevented and maybe therefore the PMN chemotactic factors C3a en C5a will not be produced.