奶牛乳腺炎源乳房链球菌关键毒力因子及调控机制研究进展OA
Research Progress on Key Virulence Factors and Regulatory Mechanisms of Streptococcus uberis in Bovine Mastitis
乳房链球菌(Streptococcus uberis)是奶牛乳腺炎中最重要的环境源性病原菌之一,具有显著的遗传多样性和环境适应能力,能在乳房组织中建立持续感染,是造成慢性和复发性乳腺炎的主要致病因素.其广泛存在于垫料、挤奶设备和牧场环境中,传播隐匿,难以根除,已成为当前乳腺炎防控中的突出挑战.尽管近年来分子生物学和多组学研究迅速发展,但乳房链球菌的毒力因子功能、相互协同关系及其上游调控网络仍缺乏系统梳理,限制了对其致病机制的整体认识.为更全面地理解乳房链球菌的致病规律,笔者以感染进程为主线,对其关键毒力因子及调控机制进行综述,按照"黏附与定植-营养获取-免疫逃逸与炎症调控-毒力调控网络"的时序逻辑展开讨论.在黏附与定植阶段,乳房链球菌黏附分子、纤维连接蛋白结合蛋白、糖酵解酶和纤溶酶原激活因子等分子介导细菌与乳腺上皮的结合与内化;在营养获取阶段,乳铁蛋白结合蛋白和锌结合蛋白参与铁、锌等必需金属离子的竞争性摄取,帮助细菌在营养免疫压力下维持代谢稳态;在免疫逃逸与炎症调控阶段,丝氨酸蛋白酶、C5a肽酶及透明质酸荚膜合成基因簇可通过抑制吞噬、调节炎症反应等方式促进感染持久化.此外,在转录调控层面,全局调控因子 Vru被证实参与多类毒力基因的表达整合,可能构成该菌毒力网络中的关键调控节点.笔者通过对现有研究证据的归纳,构建了乳房链球菌从黏附、营养竞争到免疫干扰的连续致病框架,并识别可能影响毒力表达的调控系统.通过系统总结研究进展与不足,为乳房链球菌性乳腺炎的精准防控、疫苗研发和抗毒力策略提供理论基础与研究方向.
Streptococcus uberis(S.uberis)is a major environmental pathogen responsible for bovine mastitis.Its pronounced genetic diversity and strong environmental adaptability enable the establishment of persistent intramammary infections,making it a leading cause of chronic and recurrent mastitis.The widespread presence of S.uberis in bedding materials,milking equipment,and various farm environments,together with its often subtle and difficult-to-detect transmission,presents a substantial challenge to mastitis control.Although advances in molecular biology and multi-omics technologies have accelerated,there remains a lack of systematic elucidation regarding the functions of virulence factors,their coordinated interactions,and the upstream regulatory networks in S.uberis.This gap limits a comprehensive understanding of its pathogenic mechanisms.To provide a more comprehensive understanding of the pathogenic mechanisms of S.uberis,this review summarizes its key virulence factors and regulatory mechanisms,with a focus on the course of infection:Adhesion and colonization,nutrient acquisition,immune evasion and inflammation modulation,and virulence regulation networks.During adhesion and colonization,adhesion molecules,fibronectin-binding proteins,glyceraldehyde-3-phosphate dehydrogenase,and plasminogen activators mediate attachment to and internalization into mammary epithelial cells.During nutrient acquisition,lactoferrin-binding proteins and zinc-binding proteins facilitate competitive uptake of essential metal ions,such as Fe2+and Zn2+allowing the bacterium to maintain metabolic homeostasis under nutritional immunity.In the immune evasion and inflammation-modulation phase,serine proteases,C5a peptidases,and the hyaluronic acid capsule synthesis cluster suppress phagocytosis and alter inflammatory responses,thereby promoting infection persistence.At the regulatory level,the global transcriptional regulator Vru coordinates the expression of multiple virulence-related genes and likely serves as a central node within the broader regulatory landscape.By integrating evidence across different stages of infection,this review delineates a continuous pathogenic framework in which S.uberis progresses from adhesion,nutritional competition to immune interference,and identifies regulatory systems that may affect virulence expression.The synthesis of current advances and existing knowledge gaps provides a conceptual basis for improving strategies aimed at effective mastitis control and for guiding future vaccine development and anti-virulence interventions targeting S.uberis.
郭玉玲;王文静;梁雅茜;郝海红
石河子大学动物科技学院,石河子 832000石河子大学动物科技学院,石河子 832000石河子大学动物科技学院,石河子 832000石河子大学动物科技学院,石河子 832000||华中农业大学动物医学院,武汉 430070
农业科技
乳房链球菌奶牛乳腺炎毒力因子调控机制
Streptococcus uberisbovine mastitisvirulence factorregulatory mechanism
《中国畜牧兽医》 2026 (4)
1819-1829,11
2024科技重点发展领域——牛生殖道耐药菌的快诊技术研发与示范(2024AB034)
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