Electroacupuncture promotes resolution of inflammation by modulating SPMs via vagus nerve activation in LPS-induced ALI.

IF 4.8 2区医学 Q2 IMMUNOLOGY International immunopharmacology Pub Date : 2025-02-06 Epub Date: 2025-01-01 DOI:10.1016/j.intimp.2024.113941

Yan Huang, Shuan Dong, Yuan Zhang, Ye Zhang, Yan Guo, Jia Shi, Xiangyun Li, Shasha Liu, Yong Chen, Jianbo Yu

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Abstract

During the process of acute lung injury (ALI) associated with sepsis, the α7nAChR in the cholinergic anti-inflammatory pathway (CAP) plays a crucial role. However, the roles of electroacupuncture (EA) and specialized pro-resolving mediators (SPMs) in this context remain unclear. In this study, we demonstrated that EA activates CAP via α7nAChR, reducing lung permeability and inflammatory cytokine release. Our results highlighted lipoxin A4 (LXA4) as a crucial SPM in this process. EA was shown to enhance LXA4 synthesis and alleviate symptoms in patients with sepsis-related acute respiratory distress syndrome (ARDS). Studies using α7nAChR-deficient mice confirmed its essential role in LXA4 regulation. Macrophages in bronchoalveolar lavage fluid (BALF) were identified as key contributors to the protective effects of LXA4, further supported by experiments involving pulmonary macrophage depletion. In summary, we discovered a novel anti-inflammatory pathway where EA activates α7nAChR, leading to increased LXA4 production and lung protection.

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在lps诱导的ALI中，电针通过迷走神经激活来调节SPMs，从而促进炎症的消退。

在脓毒症相关急性肺损伤（ALI）过程中，胆碱能抗炎通路（CAP）中的α7nAChR起着至关重要的作用。然而，在这种情况下，电针（EA）和专门的促溶解介质（SPMs）的作用仍不清楚。在本研究中，我们证明了EA通过α7nAChR激活CAP，降低肺通透性和炎症细胞因子的释放。我们的结果强调了脂素A4 （LXA4）在这一过程中是一个至关重要的SPM。EA可促进LXA4合成，缓解败血症相关急性呼吸窘迫综合征（ARDS）患者的症状。对α 7nachr缺陷小鼠的研究证实了其在LXA4调控中的重要作用。支气管肺泡灌洗液（BALF）中的巨噬细胞被确定为LXA4保护作用的关键贡献者，涉及肺巨噬细胞消耗的实验进一步支持了这一点。综上所述，我们发现了一种新的抗炎途径，EA激活α7nAChR，导致LXA4产生增加和肺保护。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International immunopharmacology 医学-免疫学

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.