Immunoreceptor CD300a on mast cells and dendritic cells regulates neutrophil recruitment in a murine model of sepsis
Immunoreceptor CD300a on mast cells and dendritic cells regulates neutrophil recruitment in a murine model of sepsis
复制标题
肥大细胞和树突状细胞上的免疫受体 CD300a 调节脓毒症小鼠模型中中性粒细胞的募集
DOI：
10.1093/intimm/dxw047
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发表时间：
2016
期刊：
影响因子：
4.4
通讯作者：
Shibuya A
中科院分区：
文献类型：
--
作者：
Udayanga K G S;Nakamura Y;Nakahashi-Oda C;Shibuya A
脓毒症是由机体对细菌感染的异常免疫反应引起的危及生命的综合征。虽然先天性免疫细胞在脓毒症的发病机制中是重要的，但在脓毒症期间它们的活化是如何调节的仍然不完全清楚。在这里，我们研究了抑制性免疫受体CD 300 a的作用，这是表达在各种类型的骨髓细胞，盲肠结扎穿孔（CLP）诱导的脓毒症的发病机制。为此，我们使用了在肥大细胞（MC; Cd 300 afl/flMcpt 5-Cre）、树突细胞（DC; Cd 300 afl/flItgax-Cre）或巨噬细胞和嗜中性粒细胞（Cd 300 afl/flLyz 2-Cre）上特异性缺失CD 300 a的小鼠。我们发现，CD 300 α缺失的MC或DC而不是巨噬细胞的小鼠比对照组Cd 300 afl/f小鼠存活时间显著延长。此外，尽管CD 300 a缺失MC小鼠CLP后1 h内腹腔中性粒细胞募集增加，但CD 300 a缺陷DC小鼠腹腔中性粒细胞数量直到12 h时间点才增加。这些结果表明，CD 300 α在MC和DC调节中性粒细胞募集到腹腔CLP后。
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;Cd300afl/flMcpt5-Cre), dendritic cells (DCs;Cd300afl/flItgax-Cre), or macrophages and neutrophils (Cd300afl/flLyz2-Cre). We show that mice with CD300a-deleted MCs or DCs but not macrophages survived significantly longer than did controlCd300afl/flmice. 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.