鼻窦黏膜功能重塑对生物膜诱导炎症的反应。

Remodeling of Paranasal Sinuses Mucosa Functions in Response to Biofilm-Induced Inflammation.

作者信息

Kaliniak Szczepan, Fiedoruk Krzysztof, Spałek Jakub, Piktel Ewelina, Durnaś Bonita, Góźdź Stanisław, Bucki Robert, Okła Sławomir

机构信息

Holy-Cross Cancer Center, Kielce, Poland.

Department of Medical Microbiology and Nanobiomedical Engineering, Medical University of Białystok, Białystok, Poland.

出版信息

J Inflamm Res. 2024 Feb 26;17:1295-1323. doi: 10.2147/JIR.S443420. eCollection 2024.

Abstract

Rhinosinusitis (RS) is an acute (ARS) or chronic (CRS) inflammatory disease of the nasal and paranasal sinus mucosa. CRS is a heterogeneous condition characterized by distinct inflammatory patterns (endotypes) and phenotypes associated with the presence (CRSwNP) or absence (CRSsNP) of nasal polyps. Mucosal barrier and mucociliary clearance dysfunction, inflammatory cell infiltration, mucus hypersecretion, and tissue remodeling are the hallmarks of CRS. However, the underlying factors, their priority, and the mechanisms of inflammatory responses remain unclear. Several hypotheses have been proposed that link CRS etiology and pathogenesis with host (eg, "immune barrier") and exogenous factors (eg, bacterial/fungal pathogens, dysbiotic microbiota/biofilms, or staphylococcal superantigens). The abnormal interplay between these factors is likely central to the pathophysiology of CRS by triggering compensatory immune responses. Here, we discuss the role of the sinonasal microbiota in CRS and its biofilms in the context of mucosal zinc (Zn) deficiency, serving as a possible unifying link between five host and "bacterial" hypotheses of CRS that lead to sinus mucosa remodeling. To date, no clear correlation between sinonasal microbiota and CRS has been established. However, the predominance of Corynebacteria and Staphylococci and their interspecies relationships likely play a vital role in the formation of the CRS-associated microbiota. Zn-mediated "nutritional immunity", exerted via calprotectin, alongside the dysregulation of Zn-dependent cellular processes, could be a crucial microbiota-shaping factor in CRS. Similar to cystic fibrosis (CF), the role of SPLUNC1-mediated regulation of mucus volume and pH in CRS has been considered. We complement the biofilms' "mechanistic" and "mucin" hypotheses behind CRS pathogenesis with the "structural" one - associated with bacterial "corncob" structures. Finally, microbiota restoration approaches for CRS prevention and treatment are reviewed, including pre- and probiotics, as well as Nasal Microbiota Transplantation (NMT).

摘要

鼻窦炎(RS)是鼻腔和鼻窦黏膜的急性(ARS)或慢性(CRS)炎症性疾病。CRS是一种异质性疾病,其特征在于与鼻息肉存在(CRSwNP)或不存在(CRSsNP)相关的不同炎症模式(内型)和表型。黏膜屏障和黏液纤毛清除功能障碍、炎症细胞浸润、黏液分泌过多和组织重塑是CRS的标志。然而,潜在因素、其优先级以及炎症反应的机制仍不清楚。已经提出了几种假说,将CRS的病因和发病机制与宿主因素(如“免疫屏障”)和外源性因素(如细菌/真菌病原体、生态失调的微生物群/生物膜或葡萄球菌超抗原)联系起来。这些因素之间的异常相互作用可能通过触发代偿性免疫反应而成为CRS病理生理学的核心。在这里,我们讨论鼻窦微生物群在CRS中的作用及其在黏膜锌(Zn)缺乏背景下的生物膜,作为导致鼻窦黏膜重塑的五个宿主和“细菌”CRS假说之间可能的统一联系。迄今为止,鼻窦微生物群与CRS之间尚未建立明确的相关性。然而,棒状杆菌和葡萄球菌的优势及其种间关系可能在CRS相关微生物群的形成中起重要作用。通过钙卫蛋白发挥作用的锌介导的“营养免疫”,以及锌依赖性细胞过程的失调,可能是CRS中一个关键的微生物群塑造因素。与囊性纤维化(CF)类似,已经考虑了SPLUNC1介导的对CRS中黏液体积和pH调节的作用。我们用与细菌“玉米棒”结构相关的“结构”假说补充了CRS发病机制背后生物膜的“机制”和“黏蛋白”假说。最后,综述了用于CRS预防和治疗的微生物群恢复方法,包括益生元和益生菌,以及鼻腔微生物群移植(NMT)。

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