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Department of 2 Surgery, University of Cincinnati, the 1 Shriners Hospitals for Children, and the 3 Veterans Affairs Hospital, Cincinnati, Ohio 45267-0558
Sepsis is associated with
increased intestinal permeability, but mediators and mechanisms are not
fully understood. We examined the role of interleukin (IL)-6 and IL-10
in sepsis-induced increase in intestinal permeability. Intestinal
permeability was measured in IL-6 knockout (IL-6 
/) and wild-type
(IL-6 +/+) mice 16 h after induction of sepsis by cecal ligation
and puncture or sham operation. In other experiments, mice or
intestinal segments incubated in Ussing chambers were treated with IL-6
or IL-10. Intestinal permeability was assessed by determining the
transmucosal transport of the 4.4-kDa marker fluorescein isothiocyanate
conjugated dextran and the 40-kDa horseradish peroxidase. Intestinal
permeability for both markers was increased in septic IL-6 +/+ mice but
not in septic IL-6 / mice. Treatment of nonseptic mice or of
intestinal segments in Ussing chambers with IL-6 did not influence
intestinal permeability. Plasma IL-10 levels were increased in septic
IL-6 / mice, and treatment of septic mice with IL-10 resulted in reduced intestinal permeability. Increased intestinal permeability during sepsis may be regulated by an interaction between IL-6 and
IL-10. Treatment with IL-10 may prevent the increase in mucosal permeability during sepsis.
intestine; mucosa; interleukin-6; interleukin-10
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