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补体 C5a 在失血性休克期间改变中性粒细胞的膜电位。

Complement C5a Alters the Membrane Potential of Neutrophils during Hemorrhagic Shock.

机构信息

Institute of Clinical and Experimental Trauma-Immunology, University Hospital Ulm, 89081 Ulm, Germany.

Department of Anesthesiology, University Hospital Ulm, 89081 Ulm, Germany.

出版信息

Mediators Inflamm. 2018 May 29;2018:2052356. doi: 10.1155/2018/2052356. eCollection 2018.

DOI:10.1155/2018/2052356
PMID:30002598
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5996468/
Abstract

BACKGROUND

Polymorphonuclear granulocytes (PMN) play a crucial role in host defense. Physiologically, exposure of PMN to the complement activation product C5a results in a protective response against pathogens, whereas in the case of systemic inflammation, excessive C5a substantially impairs neutrophil functions. To further elucidate the inability of PMN to properly respond to C5a, this study investigates the role of the cellular membrane potential of PMN in response to C5a.

METHODS

Electrophysiological changes in cellular and mitochondrial membrane potential and intracellular pH of PMN from human healthy volunteers were determined by flow cytometry after exposure to C5a. Furthermore, PMN from male Bretoncelles-Meishan-Willebrand cross-bred pigs before and three hours after severe hemorrhagic shock were analyzed for their electrophysiological response.

RESULTS

PMN showed a significant dose- and time-dependent depolarization in response to C5a with a strong response after one minute. The chemotactic peptide fMLP also evoked a significant shift in the membrane potential of PMN. Acidification of the cellular microenvironment significantly enhanced depolarization of PMN. In a clinically relevant model of porcine hemorrhagic shock, the C5a-induced changes in membrane potential of PMN were markedly diminished compared to healthy littermates. Overall, these membrane potential changes may contribute to PMN dysfunction in an inflammatory environment.

摘要

背景

多形核粒细胞（PMN）在宿主防御中起着至关重要的作用。在生理上，PMN 暴露于补体激活产物 C5a 会导致对病原体的保护反应，而在全身炎症的情况下，过量的 C5a 会严重损害中性粒细胞的功能。为了进一步阐明 PMN 无法正确响应 C5a 的原因，本研究探讨了 PMN 细胞膜电位在响应 C5a 时的作用。

方法

通过流式细胞术测定人健康志愿者 PMN 的细胞和线粒体膜电位以及细胞内 pH 值在暴露于 C5a 后的电生理学变化。此外，分析了雄性 Bretoncelles-Meishan-Willebrand 杂交猪在严重失血性休克前和休克后 3 小时的电生理反应。

结果

PMN 对 C5a 表现出显著的剂量和时间依赖性去极化，在一分钟后反应强烈。趋化肽 fMLP 也引起 PMN 膜电位的显著变化。细胞微环境的酸化显著增强了 PMN 的去极化。在猪失血性休克的临床相关模型中，与健康同窝仔相比，PMN 中 C5a 诱导的膜电位变化明显减弱。总的来说，这些膜电位变化可能导致炎症环境中 PMN 功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/1a5301a94a97/MI2018-2052356.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/73f4dfb3e36d/MI2018-2052356.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/5bd66c2fb6ae/MI2018-2052356.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/7955490d09cd/MI2018-2052356.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/7272258cf9c1/MI2018-2052356.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/81facd85b23c/MI2018-2052356.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/1a5301a94a97/MI2018-2052356.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/73f4dfb3e36d/MI2018-2052356.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/5bd66c2fb6ae/MI2018-2052356.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/7955490d09cd/MI2018-2052356.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/7272258cf9c1/MI2018-2052356.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/81facd85b23c/MI2018-2052356.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/5996468/1a5301a94a97/MI2018-2052356.006.jpg

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