Complement C1q inhibits the immune escape of mycobacterium tuberculosis associated with macrophage inflammation levels and glycolytic activation

IF 3.3 3区医学 Q3 IMMUNOLOGY

Microbial pathogenesis Pub Date : 2025-05-27 DOI:10.1016/j.micpath.2025.107757

Yan Liu , Jie Wang , Yonglan Pu , Shenjie Tang

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Abstract

Background

The pathogenic mechanism of mycobacterium tuberculosis (Mtb) is complex, and the immune mechanism of the host against Mtb infection and the escape mechanism of Mtb are not fully understood. This study aimed to explore the mechanisms underlying complement C1q and Mtb immune escape.

Methods

Functional experiments, using RAW264.7 cells as the focus cell line and applying CCK-8, western blotting, qRT-PCR, and flow cytometry, were carried out to uncover the exact role of C1q in macrophages, glycolytic activation, immune escape, and Mtb.

Results

C1q promoted the proliferation of RAW264.7, suppressed cell apoptosis, and regulated the secretion of M1/M2 type molecular markers in RAW264.7 cells. Moreover, C1q induced glycolytic activation in macrophages, and the immune escape of Mtb in the macrophages was accompanied by the activation of glycolysis.

Conclusion

Complement C1q inhibited the immune escape of Mtb associated with macrophage inflammation and glycolytic activation.

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补体C1q抑制与巨噬细胞炎症水平和糖酵解激活相关的结核分枝杆菌的免疫逃逸

背景结核分枝杆菌（Mtb）的致病机制复杂，宿主对结核分枝杆菌感染的免疫机制和结核分枝杆菌的逃逸机制尚不完全清楚。本研究旨在探讨补体C1q和Mtb免疫逃逸的机制。方法功能实验以RAW264.7细胞为焦点细胞系，应用CCK-8、western blotting、qRT-PCR、流式细胞术等方法，揭示C1q在巨噬细胞、糖酵解活化、免疫逃逸、结核分枝杆菌中的确切作用。结果sc1q促进RAW264.7细胞增殖，抑制细胞凋亡，调节RAW264.7细胞M1/M2型分子标记物的分泌。此外，C1q诱导巨噬细胞糖酵解激活，巨噬细胞中Mtb的免疫逃逸伴随着糖酵解激活。结论补体C1q抑制与巨噬细胞炎症和糖酵解激活相关的结核分枝杆菌的免疫逃逸。

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来源期刊

Microbial pathogenesis 医学-免疫学

CiteScore

7.40

自引率

2.60%

发文量

472

审稿时长

56 days

期刊介绍： Microbial Pathogenesis publishes original contributions and reviews about the molecular and cellular mechanisms of infectious diseases. It covers microbiology, host-pathogen interaction and immunology related to infectious agents, including bacteria, fungi, viruses and protozoa. It also accepts papers in the field of clinical microbiology, with the exception of case reports. Research Areas Include: -Pathogenesis -Virulence factors -Host susceptibility or resistance -Immune mechanisms -Identification, cloning and sequencing of relevant genes -Genetic studies -Viruses, prokaryotic organisms and protozoa -Microbiota -Systems biology related to infectious diseases -Targets for vaccine design (pre-clinical studies)