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Published on: February 9, 2014
Endogenous IL-10 protects mice from death during septic peritonitis
T van der Poll1, A Marchant, W A Buurman
1Cornell University Medical College, Department of Surgery, New York, NY 10021, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|December 1, 1995
Summary
Interleukin-10 (IL-10) production protects against lethal septic peritonitis in mice. Blocking IL-10 with antibodies increased mortality, highlighting IL-10's critical protective role in sepsis.
Area of Science:
- Immunology
- Sepsis Pathophysiology
Background:
- Interleukin-10 (IL-10) is known to inhibit Tumor Necrosis Factor (TNF) synthesis during endotoxic shock, suggesting a protective role.
- The specific function of IL-10 in septic peritonitis, a severe infection model, requires further elucidation.
Purpose of the Study:
- To investigate the role of IL-10 in the host response to septic peritonitis induced by cecal ligation and puncture (CLP).
Main Methods:
- Mice underwent CLP to induce sepsis.
- IL-10 mRNA and protein levels were measured in various organs and plasma.
- Mice were pretreated with anti-IL-10 monoclonal antibody (mAb) or control mAb.
- TNF levels, IL-1 activity, and IFN-gamma were assessed.
- Mortality rates were compared between treatment groups.
Main Results:
- CLP rapidly induced IL-10 mRNA in the liver, spleen, and lungs.
- IL-10 protein was detected in plasma post-CLP, peaking at 12 hours.
- Anti-IL-10 mAb treatment led to increased plasma TNF levels and significantly enhanced mortality.
- Anti-TNF mAb did not alter the increased mortality caused by anti-IL-10 treatment.
Conclusions:
- Septic peritonitis involves sustained IL-10 production across multiple organs.
- IL-10 plays a crucial protective role in preventing lethality during experimental septic peritonitis.
