Neutrophil IL-10 suppresses peritoneal inflammatory monocytes during polymicrobial sepsis

Journal of Leukocyte Biology

Lee M. Ocuin¹  George Plitas¹  Zubin M. Bamboat¹  Hebroon Obaid¹  Michael J. Cavnar¹  Vinod P. Balachandran¹  Ronald P. DeMatteo¹ 

[1] Hepatopancreatobiliary Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USAHepatopancreatobiliary Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USAHepatopancreatobiliary Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USA

关键词: innate immunity;    bacteria;    cytokines;    cecal ligation and puncture;   

DOI  :  10.1189/jlb.0810479

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

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.

【 授权许可】

Unknown