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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-
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-
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-
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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