脓毒症期间肝脏中CXCR2的免疫功能。
The immunological function of CXCR2 in the liver during sepsis.
作者信息
Liu Na, Bauer Michael, Press Adrian T
机构信息
Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Am Klinikum 1, 07747, Jena, Germany.
Center for Sepsis Control and Care, Jena University Hospital, Am Klinikum 1, 07747, Jena, Germany.
出版信息
J Inflamm (Lond). 2022 Nov 30;19(1):23. doi: 10.1186/s12950-022-00321-y.
BACKGROUND
The chemokine receptor CXCR2 and its ligands, especially CXCL8, are crucial mediators for the progression of liver inflammation and liver failure in sepsis. Neutrophils have the highest CXCR2 expression in mice and humans, and their activation via CXCL8 facilitates their migration to the inflamed liver for the clearance of the pathogens and, in turn, the inflammation.
MAIN BODY
In sepsis, the inflammatory insult causes extensive neutrophil migration to the liver that overwhelms the immune response. To compensate for the strong receptor activation, CXCR2 desensitizes, incapacitating the immune cells to efficiently clear pathogens, causing further life-threatening liver damage and uncontrolled pathogen spread.
CONCLUSION
CXCR2 function during infection strongly depends on the expressing cell type. It signals pro- and anti-inflammatory effects that may prompt novel cell-type-specific CXCR2-directed therapeutics.
背景
趋化因子受体CXCR2及其配体，尤其是CXCL8，是脓毒症中肝脏炎症和肝衰竭进展的关键介质。在小鼠和人类中，中性粒细胞的CXCR2表达最高，通过CXCL8激活中性粒细胞有助于其迁移至炎症肝脏以清除病原体，进而减轻炎症。
主体
在脓毒症中，炎症刺激导致大量中性粒细胞迁移至肝脏，使免疫反应不堪重负。为补偿强烈的受体激活，CXCR2脱敏，使免疫细胞无法有效清除病原体，导致进一步的危及生命的肝损伤和病原体的失控传播。
结论
感染期间CXCR2的功能强烈依赖于表达细胞类型。它发出促炎和抗炎信号，这可能促使开发新型细胞类型特异性的CXCR2导向疗法。
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