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Am J Physiol Gastrointest Liver Physiol (January 8, 2004). doi:10.1152/ajpgi.00502.2003
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Submitted on November 30, 2003
Accepted on December 30, 2003

THE ROLE OF IL-10 IN REGULATING PROINFLAMMATORY CYTOKINE RELEASE BY KUPFFER CELLS FOLLOWING TRAUMA-HEMORRHAGE

Yukihiro Yokoyama1, William C. Kitchens1, Balazs Toth1, Martin G. Schwacha1, Loring W. Rue, III1, Kirby I. Bland1, and Irshad H. Chaudry1*

1 Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.

IL-6 and TNF-{alpha} production by Kupffer cells is markedly stimulated following trauma-hemorrhage (T-H). Since IL-10 is an anti-inflammatory cytokine, the aim of this study was to determine whether IL-10 regulates Kupffer cell proinflammatory cytokine release following TH. To study thus, male adult Sprague-Dawley rats were subjected to sham operation or T-H. The procedure involved a 5cm midline laparotomy and ~90 min of hemorrhagic shock (35 mmHg), followed by resuscitation with 4x the shed blood volume in the form of Ringer's lactate. At 2 h following the end of resuscitation, livers were perfused in vitro and perfusate collected. In separate studies, Kupffer cells were isolated and incubated with different concentration of anti- IL-10 monoclonal antibodies (mAb). IgG was used as control. After 16 h of incubation, IL-6 and TNF-{alpha} levels were measured by ELISA. Plasma IL-10 levels increased significantly following T-H. IL-10 levels in the perfusate and IL-10 production by cultured Kupffer cells were also significantly higher in the T-H group. When Kupffer cells were incubated with 10 µg/ml of anti-IL-10 mAb, IL-6 and TNF-{alpha}production was significantly increased in both sham and T-H groups compared to those not treated with anti-IL-10 mAb. However, these changes were not observed when the cells were incubated with irrelevant (control) IgG. These results indicate that IL-10 production by Kupffer cells early after T-H may play a pivotal role in attenuating the proinflammatory cytokine environment, possibly in an autocrine/paracrine manner.




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