The disease burden of sepsis continues to increase, with intraabdominal contamination being a significant source of infection. Sepsis is a syndrome involving both an increase in systemic inflammation as well as a regulatory component. We have previously demonstrated that neutrophils are significant IL-10 producers in the abdomen during sepsis. Here, we sought to further characterize these neutrophils and elucidate potential underlying mechanisms resulting in IL-10 generation. Using transcriptional reporter mice, we observed that IL-10 producing neutrophils were activated, non-apoptotic, and expressed C-X-C chemokine receptor type 4-expressing. Further, we observed that active Signal Transducer and Activator of Transcription 1 expression was significantly increased in IL-10 producing versus non-IL-10 producing neutrophils. During sepsis, IFN-γ blockade lead to a decrease of neutrophil IL-10 production, while peritoneal CD4 T cells were found to be the most numerous acute producers of IFN-γ. Altogether, this report demonstrates that during sepsis, mature neutrophils can potentially dampen local inflammation by IL-10 production and this can be orchestrated by CD4 T cells through an IFN-γ dependent manner.

脓毒症的疾病负担持续增加，腹腔内污染是重要的感染源。脓毒症是一种既涉及全身炎症增加又涉及调节成分的综合征。我们之前已经证明，脓毒症期间中性粒细胞是腹部重要的 IL-10 产生者。在这里，我们试图进一步表征这些中性粒细胞并阐明导致 IL-10 生成的潜在潜在机制。使用转录报告小鼠，我们观察到产生 IL-10 的中性粒细胞被激活、非凋亡并表达 CXC 趋化因子受体 4 型。此外，我们观察到，与不产生 IL-10 的中性粒细胞相比，产生 IL-10 的中性粒细胞中活性信号转导器和转录激活剂 1 的表达显着增加。在脓毒症期间，IFN-γ 阻断导致中性粒细胞 IL-10 产生减少，而腹膜 CD4 T 细胞被发现是 IFN-γ 数量最多的急性产生者。总而言之，该报告表明，在脓毒症期间，成熟的中性粒细胞可能通过产生 IL-10 来抑制局部炎症，并且这可以由 CD4 T 细胞通过 IFN-γ 依赖性方式协调。