Journal of Inflammation Research (Feb 2024)
Remodeling of Paranasal Sinuses Mucosa Functions in Response to Biofilm-Induced Inflammation
Abstract
Szczepan Kaliniak,1 Krzysztof Fiedoruk,2 Jakub Spałek,1,3 Ewelina Piktel,2 Bonita Durnaś,1,3 Stanisław Góźdź,1,3 Robert Bucki,2,3 Sławomir Okła1,3 1Holy-Cross Cancer Center, Kielce, Poland; 2Department of Medical Microbiology and Nanobiomedical Engineering, Medical University of Białystok, Białystok, Poland; 3Institute of Medical Science, Collegium Medicum, Jan Kochanowski University of Kielce, Kielce, 25-317, PolandCorrespondence: Sławomir Okła, Department of Otolaryngology, Head and Neck Surgery, Holy-Cross Cancer Center, Kielce, 25-734, Poland, Tel/Fax +48 41 367 43 36, Email [email protected]: 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).Keywords: rhinosinusitis, chronic rhinosinusitis, nasal polyps, rhinosinusitis pathophysiology, rhinosinusitis pathophysiology, microbiota, nutritional immunity
