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Intestinal permeability is reduced and IL-10 levels are increased in septic IL-6 knockout mice
Q Wang1, C H Fang, P O Hasselgren
1Department of Surgery, the Shriners Hospitals for Children, Cincinnati, Ohio 45267-0558, USA.
Summary
Sepsis increases intestinal permeability, a process potentially mediated by interleukin-6 (IL-6) and interleukin-10 (IL-10). Findings suggest IL-10 may protect against sepsis-induced gut barrier dysfunction.
Area of Science:
- Immunology
- Gastroenterology
- Critical Care Medicine
Background:
- Sepsis is linked to heightened intestinal permeability.
- The specific molecular mediators driving this increase remain unclear.
Purpose of the Study:
- To investigate the roles of interleukin-6 (IL-6) and interleukin-10 (IL-10) in sepsis-induced intestinal hyperpermeability.
- To explore potential therapeutic strategies targeting these cytokines.
Main Methods:
- Cecal ligation and puncture (CLP) model of sepsis in wild-type and IL-6 knockout mice.
- Measurement of intestinal permeability using fluorescein isothiocyanate dextran and horseradish peroxidase.
- In vitro studies using Ussing chambers with cytokine treatment.
Main Results:
- Septic wild-type mice exhibited increased intestinal permeability, unlike septic IL-6 knockout mice.
- IL-6 administration did not affect intestinal permeability in non-septic conditions.
- Elevated plasma IL-10 levels were observed in septic IL-6 knockout mice.
- IL-10 treatment reduced intestinal permeability in septic mice.
Conclusions:
- Sepsis-induced intestinal hyperpermeability is dependent on IL-6.
- An interplay between IL-6 and IL-10 appears to regulate gut barrier function during sepsis.
- Interleukin-10 holds potential as a therapeutic agent to mitigate sepsis-related mucosal permeability increases.