Neutrophil Depletion Attenuates Human Intestinal Reperfusion Injury

Comparative anti‐inflammatory activities of antagonists to C3a and C5a receptors in a rat model of intestinal ischaemia/reperfusion injury

“…A number of chemical and cellular mediators, including reactive oxygen species (Zimmerman & Granger, 1994), platelet-activating factor Sun et al, 2000), cytokines (tumour necrosis factor-a (TNF-a) and interleukin-6) (Sorkine et al, 1995;Yao et al, 1996;Sun et al, 1999), mucosal mast cells (Kanwar & Kubes, 1994;Kanwar et al, 1998) and polymorphonuclear leukocytes (PMNs) (Hernandez et al, 1987;Sisley et al, 1994;Koike et al, 1995) have been implicated in the pathogenesis of intestinal I/R. In addition, activation of the complement system, which results in production of the biologically active anaphylatoxins, complement factors 3a (C3a), 4a and 5a (C5a), has been demonstrated to play a significant role in the pathology of I/R (Riedemann & Ward, 2003).…”

Interleukin-10 Gene Therapy Attenuates Pulmonary Tissue Injury Caused by Mesenteric Ischemia-Reperfusion in a Mouse Model

“…toration of blood flow may produce a diffuse and potentially life-threatening systemic inflammatory response, in which pulmonary injury is the most pertinent manifestation (McMillen et al 1993;Sisley et al 1994;Aytekin et al 2005). A complex group of factors such as cytokines, complement components, oxygen-free radicals, activated neutrophils and many others are believed to have a role in the development of the ischemia-reperfusion (I/R) induced pulmonary injury (Koike et al 1994;Kuzu et al 2002).…”

324 Epithelial Cell Specific MyD88 Signaling Mediates Ischemia/Reperfusion-Induced Intestinal Injury Independent of Microbial Status

“…36 Neutrophil depletion has been shown to alleviate damage in intestinal I/R-induced injury. 24,25 Interestingly, ccl2 and cxcl1 mRNA expression were reduced in Myd88 IEC−/− mice compared with control Myd88 f/f mice. This reduction correlated with a decreased infiltration of neutrophils into damaged tissue of Myd88 IEC−/− mice compared with control Myd88 f/f mice.…”

“…Multiple studies have shown a positive association between mRNA expression of Ccl2 and Cxcl1 and infiltration of neutrophils into ischemic tissue. 25,37 MyD88 signaling is essential for neutrophil recruitment and tissue damage in myocardial I/R-induced injury. 23 Victoni et al 14 also reported alleviated tissue damage in Myd88 −/− mice compared with wild-type mice and demonstrated reduced neutrophil recruitment to the intestine on I/R injury.…”