蜡样芽孢杆菌性眼内炎（Bacillus cereus endophthalmitis）是由蜡样芽孢杆菌经外源性/内源性途径感染引发的严重眼部疾病，以暴发性进展、预后不良为特征。典型临床表现为眼组织咖啡样溶解、前房咖啡色积脓及视网膜不可逆损伤，即使采用万古霉素抗感染联合玻璃体手术治疗，仍有75%～91%的患者难以恢复有效视力，约30%的患者因眼球内容物剜除或眼球摘除而致残。当前临床诊疗仍面临双重瓶颈：其一，蜡样芽孢杆菌致病机制复杂，核心因素尚未明确；其二，玻璃体切割术联合万古霉素治疗虽可延缓病程，但多数患者预后仍较差，诊疗策略有待优化。本文系统综述蜡样芽孢杆菌性眼内炎分子致病机制研究进展，基于溶细胞毒素[溶血素BL（hemolysin BL, HBL）/非溶血性肠毒素（non-hemolytic enterotoxin, NHE）/细胞毒素K（cytotoxin K, CytK）/溶血素(hemolysin）]的膜破坏作用和炎症反应、磷脂酶类的侵袭性与超氧化物歧化酶的免疫逃逸、菌体结构组分（鞭毛、菌毛、S层蛋白）致病效应以及宿主免疫应答[Toll样受体（Toll-like receptor, TLR）/NLRP3炎症小体（NLRP3 inflammasome）]失衡四个方面，整合分析国内外基础研究数据，以期为该病致病机制深度解析、靶向治疗策略探讨和转化医学前景展望等提供理论框架。

Bacillus cereus endophthalmitis is a severe ocular infection characterized by rapid progression and a poor prognosis, which can originate from either exogenous or endogenous sources. Clinically, it manifests as coffee-colored hemorrhages in ocular tissues, coffee-colored hypopyon in the anterior chamber, and irreversible retinal damage. Despite the implementation of infection control measures, such as vancomycin treatment and vitrectomy, 75%–91% of patients are unable to regain functional vision. Moreover, approximately 30% of patients require enucleation or removal of ocular contents, resulting in significant disability. The current clinical diagnosis and treatment of Bacillus cereus infections are confronted with two major challenges. Firstly, the pathogenic mechanisms are complex, and key contributing factors remain unidentified. Secondly, although vitrectomy combined with vancomycin can slow down the progression of the disease, the prognosis for most patients remains dismal, highlighting the urgent need for improved diagnostic and treatment strategies. This review conducts a systematic examination of the molecular pathogenic mechanisms of B. cereus endophthalmitis, integrating findings from both domestic and international studies. Specifically, this paper offers a comprehensive and systematic review of the latest research on the molecular pathogenic mechanisms of Bacillus cereus endophthalmitis, with a focus on four main areas: the membrane-damaging effects and inflammatory responses induced by cytolytic toxins (HBL/NHE/CytK/hemolysin); the invasiveness of phospholipases and immune evasion by superoxide dismutase; the pathogenic effects of bacterial structural components (flagella, pili, S-layer proteins);  the imbalance in host immune responses (TLR receptors/NLRP3 inflammasome). By integrating and analyzing research data from both domestic and international, this review aims to establish a theoretical framework. This framework is intended to enhance in-depth understanding of the disease’s pathogenic mechanisms, facilitate the exploration of targeted therapeutic strategies, and offer insights into the future prospects of translational medicine.