Neutrophil IL-10 suppresses peritoneal inflammatory monocytes during polymicrobial sepsis

Lee M. Ocuin, Zubin M. Bamboat, Vinod P. Balachandran, Michael J. Cavnar, Hebroon Obaid, George Plitas, Ronald P. DeMatteo

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Septic peritonitis remains a major cause of death. Neutrophils and inflammatory monocytes are principal components of the innate immune system and are essential for defense against a range of microbial pathogens. Their role and interaction in polymicrobial sepsis have not been defined clearly. Using a murine model of CLP to induce moderate sepsis, we found that neutrophil depletion did not alter survival, whereas depletion of neutrophils and inflammatory monocytes markedly reduced survival. After neutrophil depletion, inflammatory monocytes had greater phagocytic capacity and oxidative burst, and increased expression of costimulatory molecules, TNF, and iNOS. Notably, peritoneal neutrophils produced IL-10 following CLP. Adoptive i.p. transfer of WT but not IL-10-/- neutrophils into septic mice reduced monocyte expression of TNF. In vitro experiments confirmed that monocyte suppression was mediated by neutrophil-derived IL-10. Thus, during septic peritonitis, neutrophils suppress peritoneal inflammatory monocytes through IL-10 and are dispensable for survival.

Original languageEnglish
Pages (from-to)423-432
Number of pages10
JournalJournal of Leukocyte Biology
Issue number3
StatePublished - Mar 2011


  • Bacteria
  • Cecal ligation and puncture
  • Cytokines
  • Innate immunity

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology


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