B lymphocytopenia and Bregs in a not-to-die murine sepsis model.
B lymphocytopenia and Bregs in a not-to-die murine sepsis model.
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不死小鼠脓毒症模型中的 B 淋巴细胞减少症和 Bregs。
DOI：
10.1016/j.bbrc.2019.12.041
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Tanaka J.
中科院分区：
文献类型：
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作者：
Umakoshi K;Choudhury ME;Nishioka R;Matsumoto H;Abe N;Nishikawa Y;Kikuchi S;Takeba J;Yano H;Yorozuya T;Sato N;Aibiki M;Tanaka J.
脓毒症是重症监护病房中由于免疫反应失调引起的多器官衰竭而导致死亡的主要原因。在这项研究中，免疫系统的动力学变化进行了分析72小时盲肠结扎穿孔（CLP）诱导脓毒症小鼠，同时防止动物死亡，保持体温。CLP后6 h，循环中髓系细胞明显增多，B细胞明显减少。在同一时间点，出现了表达白细胞介素（IL）-10的CD 5+调节性B细胞（BCRs）。脾脏中IL-10和程序性死亡配体1（PD-L1）mRNA以及IL-1β、IL-6和干扰素γ（IFNγ）mRNA在6 h时升高。结果表明，脓毒症早期出现的B淋巴细胞减少伴Bcl-2阳性反应，可能是脓毒症免疫瘫痪的主要原因。
Sepsis is a leading cause of mortality in intensive care units due to multi-organ failure caused by dysregulated immune reactions. In this study, kinetic changes in the immune system were analyzed for 72 h in cecal ligation and puncture (CLP)-induced septic mice while preventing animal death by keeping body temperature. Increase of myeloid cells and decrease of B cells in circulation at 6 h after CLP were markedly observed. At the same time point, interleukin (IL)-10 expressing CD5+regulatory B cells (Bregs) appeared. IL-10 and programmed death-ligand 1 (PD-L1) mRNA as well as IL-1β, IL-6 and interferon γ (IFNγ) mRNA was increased in the spleen at 6 h. A gradual decrease in Bcl-2 and abrupt increase of Bim expression in the spleen at the late phase were also found. These results showed that B lymphocytopenia with the appearance of Bregs is the earliest event, likely leading to immunoparalysis in sepsis.