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从慢性感染到微生物失衡:重新思考慢性鼻窦炎

From Chronic Infection to Microbial Imbalance: Rethinking Chronic Rhinosinusitis.

综述 Meta鼻科IF 6.3Q1

文献信息

中文摘要

慢性鼻窦炎(CRS)传统上被视为一种慢性炎症性疾病,其中涉及微生物因素。然而,越来越多的证据表明,将CRS理解为鼻窦微生物稳态的破坏,而非由单一病原体引起的慢性感染,可能更为恰当。本综述总结了关于健康鼻窦微生物组的组成与功能以及CRS中微生物改变的最新认识。特别关注涉及潜在致病微生物(包括金黄色葡萄球菌和铜绿假单胞菌)的菌群失调,以及生物膜形成及其与上皮屏障和宿主免疫反应的相互作用。我们还讨论了可能促成微生物失衡的宿主相关、治疗、激素和环境因素。目前的证据尚不能明确确定菌群失调是慢性炎症的原因还是结果。基于此处综合的证据,我们提出CRS可被理解为微生物失衡与慢性炎症之间动态的双向相互作用,其中微生物改变可能促成上皮和免疫失调,而宿主环境的变化则影响鼻窦生态系统。通过整合这些微生物学和宿主相关视角,本综述为理解CRS病理生理学和指导未来对鼻窦微生物稳态个体模式的研究提供了一个更广阔的框架。

英文摘要

Chronic rhinosinusitis (CRS) has traditionally been viewed as a chronic inflammatory disease in which microbial factors are implicated. However, increasing evidence suggests that CRS may be better understood as a disruption of sinonasal microbial homeostasis rather than as a chronic infection caused by a single pathogen. This review summarizes current knowledge on healthy sinonasal microbiome composition and function as well as microbial alterations in CRS. Particular attention is given to dysbiosis involving potentially pathogenic microorganisms, including Staphylococcus aureus and Pseudomonas aeruginosa, as well as biofilm formation and its interactions with the epithelial barrier and host immune response. We also discuss host-related, therapeutic, hormonal, and environmental factors that may contribute to microbial imbalance. Current evidence does not clearly establish whether dysbiosis is a cause or consequence of chronic inflammation. Based on the evidence synthesized here, we propose that CRS may be understood as a dynamic, bidirectional interaction between microbial imbalance and chronic inflammation, whereby microbial alterations may contribute to epithelial and immune dysregulation, while changes in the host environment influence the sinonasal ecosystem. By integrating these microbiological and host-related perspectives, this review provides a boarder framework for understanding CRS pathophysiology and guiding future research into individual patterns of sinonasal microbial homeostasis.