Surgical stress quickly affects the numbers of circulating B-cells and neutrophils in murine septic and aseptic models through a β2 adrenergic receptor
Surgical stress quickly affects the numbers of circulating B-cells and neutrophils in murine septic and aseptic models through a β2 adrenergic receptor
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手术应激通过 β2 肾上腺素能受体快速影响小鼠败血症和无菌模型中循环 B 细胞和中性粒细胞的数量
DOI：
10.1080/1547691x.2022.2029630
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发表时间：
2022
影响因子：
3.3
通讯作者：
Junya Tanaka
中科院分区：
文献类型：
--
作者：
Ryutaro Nishioka;Yusuke Nishi;Mohammed E. Choudhury;Riko Miyaike;Ayataka Shinnishi;Kensuke Umakoshi;Yasutsugu Takada;Norio Sato;Mayuki Aibiki;Hajime Yano;Junya Tanaka
脓毒症是一种伴随着循环中髓样细胞增加和淋巴样细胞减少的病理。在盲肠结扎穿孔（CLP）诱导的小鼠脓毒症模型中，循环中中性粒细胞数量增加和B细胞水平降低是免疫系统中最早的变化。然而，迄今为止，这些变化的机制仍有待阐明。本研究旨在阐明CLP后白细胞水平变化的机制，并确定交感神经系统（SNS）参与的作用。在此，雄性C57/BL 6小鼠经受CLP或假CLP（腹壁切开，但盲肠未被穿刺）。然后使用流式细胞术研究循环白细胞数量随时间的变化。结果表明，假CLP导致循环中多形核细胞（PMN;其中大部分是中性粒细胞）增加和B细胞减少，其程度与CLP诱导的相似。肾上腺素能激动剂和拮抗剂的作用，以及肾上腺切除术，也进行了检查，在小鼠CLP或假CLP。在处死前3 h给予肾上腺素或β 2肾上腺素能受体激动剂（克伦特罗），产生的变化与假CLP后2 h观察到的变化几乎相同。而在CLP前1h或假CLP后2 h给予β 2肾上腺素能受体拮抗剂ICI 118，551则抑制了预期的变化。去甲肾上腺素和α1肾上腺素能受体激动剂去氧肾上腺素没有产生显着作用。肾上腺切除术前24小时假CLP显着取消了预期的假CLP诱导的变化之前看到的。克伦特罗增加Cxcr 4（趋化因子受体基因）的脾细胞表达;肾上腺切除术废除假CLP诱导的Cxcr 4表达。CXCR 4拮抗剂AMD 3100抑制假CLP诱导的变化。从这些结果可以得出结论，脓毒症诱导的SNS激活可能是脓毒症中免疫功能障碍的一个原因-无论发病过程如何。
Sepsis is a pathology accompanied by increases in myeloid cells and decreases in lymphoid cells in circulation. In a murine sepsis model induced by cecum ligation and puncture (CLP), increasing numbers of neutrophils and decreasing levels of B-cells in circulation are among the earliest changes in the immune system. However, to date, the mechanisms for these changes remain to be elucidated. The study here sought to elucidate mechanisms underlying the changes in the leukocyte levels after CLP and also to determine what, if any, role for an involvement of the sympathetic nervous system (SNS). Here, male C57/BL6 mice were subjected to CLP or sham-CLP (abdominal wall incised, but cecum was not punctured). The changes in the number of circulating leukocytes over time were then investigated using flow cytometry. The results showed that a sham-CLP led to increased polymorphonuclear cells (PMN; most of which are neutrophils) and decreased B-cells in the circulation to an extent similar to that induced by CLP. Effects of adrenergic agonists and antagonists, as well as of adrenalectomy, were also examined in mice that underwent CLP or sham-CLP. Administering adrenaline or a β2adrenergic receptor agonist (clenbuterol) to mice 3 h before sacrifice produced almost identical changes to as what was seen 2 h after performing a sham-CLP. In contrast, giving a β2adrenergic receptor antagonist ICI118,551 1 h before a CLP or sham-CLP suppressed the expected changes 2 h after the operations. Noradrenaline and an α1 adrenergic receptor agonist phenylephrine did not exert significant effects. Adrenalectomy 24 h before a sham-CLP significantly abolished the expected sham-CLP-induced changes seen earlier. Clenbuterol increased splenocyte expression ofCxcr4(a chemokine receptor gene); adrenalectomy abolished sham-CLP-inducedCxcr4expression. A CXCR4 antagonist AMD3100 repressed the sham-CLP-induced changes. From these results, it may be concluded that sepsis-induced activation of the SNS may be one cause for immune dysfunction in sepsis – regardless of the pathogenetic processes.
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