Zhang Xindan, Zhang Duo, Zhou Di, Zheng Shuai, Li Shuang, Hou Qinlong, Li Gen, Han Huiming
The School of Basic Medicine, Beihua University, Jilin, China.
The Center for Infection and Immunity, Beihua University, Jilin, China.
Front Microbiol. 2025 Jul 21;16:1619626. doi: 10.3389/fmicb.2025.1619626. eCollection 2025.
() is a ubiquitous opportunistic pathogen and a major cause of nosocomial infections worldwide. It can provoke a spectrum of clinical manifestations-ranging from postoperative wound infections, pressure ulcers, abscesses, and otitis media to life-threatening bacteremia and sepsis, especially in burn patients. Over the past decade, extensive research has elucidated its complex virulence repertoire, including exotoxins, proteases, and siderophores; the hierarchical Quorum Sensing (QS) networks; and its robust capacity for biofilm formation. In this review, we consolidate significant studies published since 2015 to develop a comprehensive framework elucidating the virulence mechanisms of . Beyond cataloging individual factors, we highlight how QS regulators coordinate toxin production and biofilm maturation, and how these processes converge to facilitate immune evasion. We further examine cross-talk between QS circuits (Las, Rhl, and Pqs), their response to environmental cues, and the modulatory role of host signals. Despite these advances, significant gaps remain: the spatiotemporal interplay among different virulence modules; the precise molecular triggers of biofilm dispersal; and the dynamics of bacterial-host immune interactions . Notably, targeting QS with small-molecule inhibitors has shown promise in attenuating pathogenicity, yet translating these findings into clinical therapies requires more nuanced understanding of resistance emergence and host microbiome effects. We propose that future investigations prioritize (1) the structural biology of QS receptors to guide rational inhibitor design; (2) single-cell and organ-on-a-chip models to dissect biofilm heterogeneity; (3) dual-omics approaches to map host-pathogen signaling crosstalk; and (4) environmental modulators-such as iron availability and shear stress-that fine-tune virulence expression. Such multidisciplinary efforts will underpin the development of next-generation anti-virulence therapies, ultimately improving prevention and treatment of infections and safeguarding public health.
（某病原体名称）是一种普遍存在的机会致病菌，是全球医院感染的主要原因。它可引发一系列临床表现，从术后伤口感染、压疮、脓肿、中耳炎到危及生命的菌血症和败血症，尤其是在烧伤患者中。在过去十年中，广泛的研究阐明了其复杂的毒力机制，包括外毒素、蛋白酶和铁载体；分级群体感应（QS）网络；以及其强大的生物膜形成能力。在本综述中，我们整合了自2015年以来发表的重要研究，以建立一个全面的框架来阐明（某病原体名称）的毒力机制。除了列举个体因素外，我们还强调了QS调节因子如何协调毒素产生和生物膜成熟，以及这些过程如何协同促进免疫逃逸。我们进一步研究了QS回路（Las、Rhl和Pqs）之间的相互作用、它们对环境线索的反应以及宿主信号的调节作用。尽管取得了这些进展，但仍存在重大差距：不同毒力模块之间的时空相互作用；生物膜分散的确切分子触发因素；以及细菌与宿主免疫相互作用的动态变化。值得注意的是，用小分子抑制剂靶向QS在减弱致病性方面已显示出前景，但将这些发现转化为临床治疗需要更细致地了解耐药性的出现和宿主微生物群的影响。我们建议未来的研究优先考虑：（1）QS受体的结构生物学，以指导合理的抑制剂设计；（2）单细胞和芯片器官模型，以剖析生物膜的异质性；（3）双组学方法，以绘制宿主-病原体信号相互作用图谱；（4）环境调节因子，如铁的可用性和剪切应力，它们可微调毒力表达。这种多学科努力将为下一代抗毒力疗法的发展奠定基础，最终改善（某病原体名称）感染的预防和治疗，并保障公众健康。
