Abstract
The prevalence of reactive nasal inflammatory conditions, for example, allergic rhinitis and chronic rhinosinusitis, is steadily increasing in parallel with significant environmental changes worldwide. Allergens and as yet undefined environmental agents may trigger these conditions via the involvement of host intrinsic factors, including the innate and adaptive immune system, the nasal epithelium, and the nasal nervous system. The critical role of the nasal microbiota in coordinating these components has emerged in recent studies documenting a significant association between microbial composition and the onset and progression of allergic or nonallergic inflammation. It is now clear that the local microbiota is a major player in the development of the mucosa-associated lymphoid tissue and in the regulation of such adaptive responses as IgA production and the function of effector and regulatory T cells. Microbial components also play a major role in the regulation of epithelial barrier functions, including mucus production and the control of paracellular transport across tight junctions. Bacterial components, including lipopolysaccharide, have also been shown to induce or amplify neuroinflammatory responses by engaging specific nociceptors. Finally, bacterial products may promote tissue remodeling processes, including nasal polyp formation, by interacting with formyl peptide receptors and inducing the expression of angiogenic factors and matrix-degrading enzymes.
Highlights
The nose, the uppermost portion of the respiratory tract, serves important physiologic functions, such as air filtration, warming, humidification, and olfaction
Remodeling in this condition is characterized by excessive collagen production and thickening of the extracellular matrix [157]. This process is mediated by transforming growth factor- (TGF-)β, which is distinctly upregulated in the CRSsNP mucosa relative to CRS with nasal polyps (CRSwNP) [157]. These findings present important therapeutic implications, in that, while T helper cell- (Th2-)driven eosinophilic inflammation and polyp formation are relatively well controlled with, and at least partly reversed by, inhaled corticosteroids, Th17-dependent inflammation and TGF-β-mediated remodeling are not [171,172,173]
Regardless, it can be concluded that the barrier function of the nasal mucosa, or mucosal firewall, represents the key element linking nasal dysbiosis to the cellular and molecular processes that lead to and sustain inflammation
Summary
The nose, the uppermost portion of the respiratory tract, serves important physiologic functions, such as air filtration, warming, humidification, and olfaction It consists of two cavities or fossae extending from the external nostrils (anterior nares) to the choanae and separated longitudinally by an osteocartilaginous septum. If the anatomy and physiology of the nasal cavities are complex, at least as complex are the pathophysiological processes that underlie the onset and progression of reactive nasal inflammatory conditions These include a heterogeneous group of disorders, ranging from seasonal allergic rhinitis to nonallergic, persisting, refractory forms of chronic. Regardless, a number of common factors variably contribute to favoring and worsening the inflammatory response in these reactive nasal conditions [7,8,9] These include the innate and adaptive immune system, the epithelial barrier function, a neuroinflammatory component (i.e., neurogenic inflammation), tissue remodeling processes, and the nasal microbiota. We will touch on some of these studies in parallel with discussing more recent acquisitions in allergic rhinitis and related reactive nasal inflammatory conditions
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