Interacting neuroendocrine and innate and acquired immune pathways regulate neutrophil mobilization from bone marrow following hemorrhagic shock.
Interacting neuroendocrine and innate and acquired immune pathways regulate neutrophil mobilization from bone marrow following hemorrhagic shock.
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DOI：
10.4049/jimmunol.182.1.572
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发表时间：
2009-01-01
影响因子：
4.4
通讯作者：
Fan, Jie
中科院分区：
文献类型：
--
作者：
Liu, Yujian;Yuan, Youzhong;Li, Yuehua;Zhang, Jian;Xiao, Guozhi;Vodovotz, Yoram;Billiar, Timothy R.;Wilson, Mark A.;Fan, Jie
多形核中性粒细胞 (PMN) 是重要的先天免疫效应细胞，它可以保护宿主，也可以通过迁移到受伤或发炎的组织来加剧器官功能障碍。重大创伤后的复苏性失血性休克 (HS/R) 通过引发 PMN 迁移和激活来响应第二次（通常是微不足道的）刺激（所谓的“双重打击”现象），从而促进器官炎症的发展。骨髓 (BM) 中的中性粒细胞 (PMN) 动员支持中性粒细胞 (HS/R) 持续的、由 HS/R 引发的迁移。我们讨论了 HS/R 在调节 BM 中 PMN 出口方面的作用和机制。我们证明HS/R通过警报素HMGB1以自分泌和TLR4信号依赖的方式诱导巨噬细胞分泌IL-23，反过来，IL-23通过IL-17-G-CSF介导的机制诱导PMN从BM中流出。我们还表明，巨噬细胞儿茶酚胺激活 β-肾上腺素能受体介导 HS/R 诱导的 HMGB1 释放。这些数据表明，HS/R 作为一种全局缺血/再灌注刺激，通过一系列相互作用的途径（包括神经内分泌以及先天性和后天性免疫系统）调节 PMN 动员。阻断这一新的信号轴可能为创伤后炎症提供新的治疗靶点。
Polymorphonuclear neutrophils (PMN) are critical innate immune effector cells that either protect the host or exacerbate organ dysfunction by migrating to injured or inflamed tissues. Resuscitated hemorrhagic shock (HS/R) following major trauma promotes the development of organ inflammation by priming PMN migration and activation in response to a second, often trivial, stimulus (a so-called “two hit” phenomenon). PMN mobilization from bone marrow (BM) supports a sustained, HS/R-primed migration of PMN. We addressed the role and mechanism of HS/R in regulating PMN egress from BM. We demonstrate that HS/R through the alarmin HMGB1 induces IL-23 secretion from macrophages in an autocrine and TLR4 signaling-dependent manner, in turn, IL-23, through an IL-17-G-CSF-mediated mechanism induces PMN egress from BM. We also show that β-adrenergic receptor activation by catecholamine of macrophages mediates the HS/R-induced release of HMGB1. These data indicate that HS/R, a global ischemia/reperfusion stimulus, regulates PMN mobilization through a series of interacting pathways that include neuro-endocrine and innate and acquired immune systems. Blocking this novel signaling axis may present a novel therapeutic target for post-trauma inflammation.
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影响因子：
15.9
作者：
Becker, C;Wirtz, S;Neurath, MF
通讯作者：
Neurath, MF
DOI：
10.1152/ajplung.00359.2004
发表时间：
2005-05-01
影响因子：
4.9
作者：
Kim, JY;Park, JS;Abraham, E
通讯作者：
Abraham, E
影响因子：
4.4
作者：
Fan, J;Kapus, A;Rotstein, OD
通讯作者：
Rotstein, OD
影响因子：
4.4
作者：
Fan, Jie;Li, Yuehua;Wilson, Mark A.
通讯作者：
Wilson, Mark A.
影响因子：
4.8
作者：
Huttunen, HJ;Fages, C;Rauvala, H
通讯作者：
Rauvala, H