巨噬细胞在败血症诱发的急性肝损伤中的免疫作用

IF 4.8 2区 医学 Q2 IMMUNOLOGY International immunopharmacology Pub Date : 2024-10-29 DOI:10.1016/j.intimp.2024.113492
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引用次数: 0

摘要

脓毒症诱发的急性肝损伤(SALI)是脓毒症多器官功能障碍综合征的一种表现形式,与预后不良和高死亡率有关。肝巨噬细胞亚群的多样性和可塑性解释了它们在不同肝病中的不同功能反应。Kupffer 巨噬细胞、肝囊巨噬细胞和单核细胞衍生巨噬细胞参与病原体的识别和清除以及炎症反应的调节,通过不同的热噬、铁噬和自噬途径加剧 SALI 的进展。同时,它们在维持肝脏稳态以及 SALI 损伤和修复过程中也发挥着重要作用。其他巨噬细胞在病理条件下被招募到病变组织,并在信号分子、转录因子和代谢重编程的影响下极化成各种表型(主要是 M1 和 M2 型),从而发挥不同的作用和功能。本综述概述了巨噬细胞在 SALI 中的免疫作用,并讨论了巨噬细胞在肝损伤和修复中的多重作用,为今后的研究提供参考。
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Immunologic role of macrophages in sepsis-induced acute liver injury
Sepsis-induced acute liver injury (SALI), a manifestation of sepsis multi-organ dysfunction syndrome, is associated with poor prognosis and high mortality. The diversity and plasticity of liver macrophage subpopulations explain their different functional responses in different liver diseases. Kupffer macrophages, liver capsular macrophages, and monocyte-derived macrophages are involved in pathogen recognition and clearance and in the regulation of inflammatory responses, exacerbating the progression of SALI through different pathways of pyroptosis, ferroptosis, and autophagy. Concurrently, they play an important role in maintaining hepatic homeostasis and in the injury and repair processes of SALI. Other macrophages are recruited to diseased tissues under pathological conditions and are polarized into various phenotypes (mainly M1 and M2 types) under the influence of signaling molecules, transcription factors, and metabolic reprogramming, thereby exerting different roles and functions. This review provides an overview of the immune role of macrophages in SALI and discusses the multiple roles of macrophages in liver injury and repair to provide a reference for future studies.
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来源期刊
CiteScore
8.40
自引率
3.60%
发文量
935
审稿时长
53 days
期刊介绍: International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome. The subject material appropriate for submission includes: • Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders. • Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state. • Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses. • Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action. • Agents that activate genes or modify transcription and translation within the immune response. • Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active. • Production, function and regulation of cytokines and their receptors. • Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.
期刊最新文献
Corrigendum to "mTOR aggravated CD4+ T cell pyroptosis by regulating the PPARγ-Nrf2 pathway in sepsis" [Int. Immunopharmacol. 140 (2024) 112822]. Corrigendum to "Role of glucose metabolism reprogramming in keratinocytes in the link between psoriasis and metabolic syndrome" [Int. Immunopharmacol. 139 (2024) 112704]. Isoamericanin A ameliorates neuronal damage and alleviates vascular cognitive impairments by inhibiting oxidative stress through activation of the Nrf2 pathway. Neuroprotective effects of gypenosides on LPS-induced anxiety and depression-like behaviors. Corrigendum to "Artesunate ameliorates ligature-induced periodontitis by attenuating NLRP3 inflammasome-mediated osteoclastogenesis and enhancing osteogenic differentiation" [Int. Immunopharmacol. 123 (2023) 110749].
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