“…LPS has many biological effects that could contribute to intestinal graft damage including: (1) activation of neutrophils to produce elastase and superoxide ions that damage endothelial cells [9], (2) increased surface expression of the adhesion molecules such as CD11-CD18 that promote the adherence of leukocytes to the endothelium [9], and ( 3 ) stimulation of macrophages to release proinflammatory cytokines such as TNF-a, IL-1, and IL-6 [14,17]. TNF-a is cytotoxic to intestinal epithelial cells [3]; it also damages gut barrier function [16], activates neutrophils, stimulates procoagulant activity, and increases the expression of MHC antigens [ll]. TNF-a may play a central role in the pathogenesis of intestinal allograft rejection since treatment with anti-TNF-a antibodies has prolonged small bowel allograft survival in rats [19].…”