Immunoreceptor CD300a on mast cells and dendritic cells regulates neutrophil recruitment in a murine model of sepsis

Sepsis is a life-threatening syndrome caused by abnormal host immune responses against bacterial infection. Although innate immune cells are known to be important in the pathogenesis of sepsis, how their activation is regulated during sepsis remains incompletely understood. Here, we examined the role of the inhibitory immunoreceptor CD300a, which is expressed on various types of myeloid cells, in the pathogenesis of sepsis induced by cecal ligation and puncture (CLP). To this end, we used mice in which CD300a was specifically deleted on mast cells (MCs; Cd300a ^fl/flMcpt5-Cre), dendritic cells (DCs; Cd300a ^fl/flItgax-Cre), or macrophages and neutrophils (Cd300a ^fl/flLyz2-Cre). We show that mice with CD300a-deleted MCs or DCs but not macrophages survived significantly longer than did control Cd300a ^fl/fl mice. In addition, whereas neutrophil recruitment into the peritoneal cavity was increased within 1 h after CLP in mice with CD300a-deleted MCs, peritoneal neutrophils did not increase in number until the 12 h time point in mice with CD300a-deficient DCs. These results indicate that CD300a on MCs and DCs regulates neutrophil recruitment into the peritoneal cavity after CLP.

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