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Curr Infect Dis Rep (2011) 13:159168
DOI 10.1007/s11908-011-0166-z
Chronic Rhinosinusitis as a Multifactorial Inflammatory Disorder
Stella Lee & Andrew P. Lane
Published online: 1 February 2011# Springer Science+Business Media, LLC 2011
Abstract Chronic rhinosinusitis (CRS) is a prevalent health condition characterized by sinonasal mucosal inflammation lasting at least 12 weeks. Heterogeneous in clinical presentation, histopathology, and therapeutic response, CRS represents a spectrum of disease entities with variable pathophysiology. Increased knowledge of cellular and molecular derangements in CRS suggests potential etiologies and targets for therapy. Microbial elements including fungi, staphylococcal enterotoxin, and biofilms have been implicated as inflammatory stimuli, along with airborne irritants and allergens. Defects in innate immunity have gained increased attention as contributors to the chronic inflammatory state. A combination of host susceptibility and environmental exposure is widely believed to underlie CRS, although direct evidence is lacking. Presently, without precise disease definitions and identifiable universal triggers, CRS pathogenesis is broadly described as multifactorial. Current research is beginning to unravel complex and diverse effects of chronic inflammation on sinonasal mucosal homeostasis, but dysfunctional pathways of inflammatory regulation and resolution require further elucidation.
Keywords Chronic rhinosinusitis . Inflammation . Innate immunity. Host defense . Epithelium
Introduction
Despite its prevalence and significant health impact, the etiology of chronic rhinosinusitis (CRS) remains incompletely understood. Unlike acute bacterial sinusitis, for which the pathophysiology is well-defined, CRS is a heterogeneous condition characterized broadly by persistent inflammation of the sinonasal mucosa [1]. It is widely believed that the causes of inflammation in CRS are diverse and multifactorial, relating to overlapping host and environmental triggers. Disruption of normal epithelial function subsequent to inflammation of any origin can result in mucostasis and microbial colonization. Infection, in turn, stimulates further inflammation and exacerbates the chronic disease process. Current research in the field has attempted to elucidate the factors driving persistent sinonasal inflammation [2], highlighting the complex interplay between the environment and innate and adaptive mucosal immune mechanisms [3]. It is increasingly recognized that CRS is not a single disease entity, but instead varies widely in clinical presentation, histopathology, and response to therapy. Multiple pathophysiologic pathways likely exist that can result in the common endpoint of sinonasal mucosal inflammation (Fig. 1). Perhaps more importantly, once chronic inflammation becomes manifest, secondary activation of additional pathophysiologic...