Xu Yuhua, Ma Xi, Wu Zhifeng, Huang Ruitong, Liao Chenhua, Huang Di, Tang Yujun, Zhu Chengbin, Wang Yaqi, Zhang Siyuan, Liu Peng, Peng Jiaofeng
Institute of Pathogenic Biology, Basic Medical School, Hengyang Medical School, Hengyang Central Hospital, University of South China, Hengyang, Hunan, China.
Plastic Surgery Department, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Front Microbiol. 2025 Jun 26;16:1621137. doi: 10.3389/fmicb.2025.1621137. eCollection 2025.
SUMOylation, the covalent attachment of small ubiquitin-like modifier proteins (SUMO) to lysine residues of target substrates, has emerged as a crucial post-translational modification regulating various cellular processes. Recent studies have revealed that SUMOylation also plays significant roles in host-pathogen interactions during bacterial infections. On the one hand, SUMOylation can modulate host innate immune responses, such as inflammatory signaling and autophagy, to defend against invading bacteria. On the other hand, certain bacterial pathogens have evolved strategies to exploit or manipulate the host SUMOylation machinery to promote their survival and replication. Some bacterial effector proteins directly target host SUMO enzymes or SUMO-conjugated substrates to disrupt host defense mechanisms. This review summarizes the current understanding of the complex interplay between SUMOylation and bacterial infection, highlighting the dual roles of SUMOylation in host defense and bacterial pathogenesis. We discuss the mechanisms by which SUMOylation regulates host immune responses against bacterial infection and how bacterial pathogens hijack host SUMOylation for their own benefit. Moreover, we explore the potential of targeting SUMOylation as a novel therapeutic strategy for combating bacterial infections. Further research into the intricate relationship between SUMOylation and bacterial infection may provide valuable insights for developing innovative anti-infective therapies.
SUMO化，即小泛素样修饰蛋白（SUMO）与靶底物赖氨酸残基的共价连接，已成为一种调节各种细胞过程的关键翻译后修饰。最近的研究表明，SUMO化在细菌感染期间的宿主-病原体相互作用中也发挥着重要作用。一方面，SUMO化可以调节宿主的固有免疫反应，如炎症信号传导和自噬，以抵御入侵的细菌。另一方面，某些细菌病原体已经进化出利用或操纵宿主SUMO化机制以促进其存活和复制的策略。一些细菌效应蛋白直接靶向宿主SUMO酶或SUMO共轭底物，以破坏宿主防御机制。本综述总结了目前对SUMO化与细菌感染之间复杂相互作用的理解，强调了SUMO化在宿主防御和细菌发病机制中的双重作用。我们讨论了SUMO化调节宿主针对细菌感染的免疫反应的机制，以及细菌病原体如何为自身利益劫持宿主SUMO化。此外，我们探讨了将靶向SUMO化作为对抗细菌感染的新型治疗策略的潜力。对SUMO化与细菌感染之间复杂关系的进一步研究可能为开发创新的抗感染疗法提供有价值的见解。
