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Articles in PresS, published online ahead of print March 29, 2002
J Appl Physiol, 10.1152/jap.00159.2002
Submitted on February 27, 2002
Accepted on March 25, 2002
1 Department of Anesthesia, Brigham and Women's Hospital, Boston, MA, USA
2 Department of Pathology, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: gstahl{at}zeus.bwh.harvard.edu.
Gastrointestinal ischemia/reperfusion (GI/R) injury is often associated with remote tissue injury. Complement activation plays an important role in the local and remote tissue injury associated with GI/R. We developed a new murine model of gastrointestinal I/R that has complement-dependent local and remote tissue injury. Twenty, but not thirty, min of gastrointestinal ischemia followed by 3 hrs of reperfusion induced a significant loss of intestinal lactate dehydrogenase that was significantly prevented by a murine anti-murine C5 mAb. Anti-C5 also significantly decreased neutrophil (PMN) infiltration into the gut and lung. GI/R significantly increased pulmonary ICAM-1 mRNA and protein expression that was significantly inhibited by anti-C5. Pulmonary MIP-2 mRNA was significantly induced by GI/R and inhibited by anti-C5 treatment. These data demonstrate that brief periods of murine gastrointestinal I/R activate complement, leading to tissue injury and PMN accumulation. Anti-C5 treatment attenuates tissue injury, PMN recruitment, and leukocyte adherence molecule and chemokine expression in the mouse. This model will be well suited to investigate the role of complement mediate tissue injury and gene expression following GI/R.
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