Xiang Miao, Li Panpan, Yue Xiaofei, Liu Linlin, Wang Linjing, Sun Nengjin, Wang Kaile, Zhang Yuying, Wang Hongyan
Key Laboratory of Immune Microenvironment and Inflammatory Disease Research in Universities of Shandong Province, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, China.
Department of Pathogenic Biology, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, China.
Front Immunol. 2025 Aug 4;16:1636768. doi: 10.3389/fimmu.2025.1636768. eCollection 2025.
() is a microaerophilic, gram-negative spirochete that primarily colonizes the human gastric mucosa. It is strongly linked to gastritis, ulcers, and the development of malignant tumors. Macrophages, as one of the key components of the innate immune system, play a crucial role in maintaining immune homeostasis through a range of functions, including pathogen phagocytosis, antigen recognition and presentation, inflammation regulation and tumor immune surveillance. Emerging evidence suggests that employs diverse molecular mechanisms to evade immune clearance by macrophages. This review provides a comprehensive analysis of how infection modulates macrophage functions, including impairing pathogen recognition and phagocytosis, disrupting phagosome maturation and reducing immune clearance capacity. Furthermore, infection skews macrophage polarization to promote chronic inflammatory damage, inhibits antigen processing and presentation to evade adaptive immune responses and induces macrophage apoptosis via activation of apoptotic signaling pathways. By unraveling the complex molecular interactions between and macrophages, this review highlights strategies for reprogramming macrophage functions, offering innovative approaches to address the limitations of conventional antimicrobial therapies and advancing targeted therapeutic interventions for -associated diseases.
()是一种微需氧的革兰氏阴性螺旋体,主要定殖于人类胃黏膜。它与胃炎、溃疡及恶性肿瘤的发生密切相关。巨噬细胞作为固有免疫系统的关键组成部分之一,通过一系列功能在维持免疫稳态中发挥关键作用,这些功能包括病原体吞噬、抗原识别与呈递、炎症调节及肿瘤免疫监视。新出现的证据表明,()利用多种分子机制逃避巨噬细胞的免疫清除。本综述全面分析了()感染如何调节巨噬细胞功能,包括损害病原体识别与吞噬、破坏吞噬体成熟及降低免疫清除能力。此外,()感染使巨噬细胞极化偏向促进慢性炎症损伤,抑制抗原加工与呈递以逃避适应性免疫反应,并通过激活凋亡信号通路诱导巨噬细胞凋亡。通过揭示()与巨噬细胞之间复杂的分子相互作用,本综述强调了重编程巨噬细胞功能的策略,为解决传统抗菌疗法的局限性及推进针对()相关疾病的靶向治疗干预提供了创新方法。