TY - JOUR
T1 - Perspectives on the etiology of chronic rhinosinusitis
T2 - An immune barrier hypothesis
AU - Kern, Robert C.
AU - Conley, David B.
AU - Walsh, William
AU - Chandra, Rakesh
AU - Kato, Atsushi
AU - Tripathi-Peters, Anju
AU - Grammer, Leslie C.
AU - Schleimer, Robert P.
PY - 2008
Y1 - 2008
N2 - Background: Chronic rhinosinusitis (CRS) has been defined as persistent symptomatic inflammation of the nasal and sinus mucosa resulting from the interaction of multiple host and environmental factors. Recent studies have implicated Alternaria fungi or toxigenic Staphylococcus aureus as critical agents in CRS pathogenesis. The emphasis on environmental agents in CRS etiology has focused interest toward elimination of those agents as the prime mechanism of therapy. This viewpoint is in marked contrast to the current perspective on some other chronic inflammatory epithelial disorders that afflict the skin, lungs, and gut, wherein host factors are believed to predispose to disease expression in the presence of ubiquitous environmental agents. Methods: The current review evaluates CRS etiology from this perspective and considers that CRS develops, in part, as an outcome of a dysfunctional host response. Specifically, evidence from our laboratory and others will be reviewed indicating that CRS is associated with a failure of the mechanical and immunologic barriers across the nasal mucosa. The hypothesis would further propose that genetic and epigenetic variation predisposes susceptible individuals to barrier failure in the presence of environmental stress leading to CRS. Results: From this unifying perspective, bacteria and fungi are seen as disease modifiers rather than primary etiologic agents. Conclusion: The goal is to place concepts of CRS pathophysiology in a framework consistent with a current understanding of chronic inflammation in general and epithelial disease in particular.
AB - Background: Chronic rhinosinusitis (CRS) has been defined as persistent symptomatic inflammation of the nasal and sinus mucosa resulting from the interaction of multiple host and environmental factors. Recent studies have implicated Alternaria fungi or toxigenic Staphylococcus aureus as critical agents in CRS pathogenesis. The emphasis on environmental agents in CRS etiology has focused interest toward elimination of those agents as the prime mechanism of therapy. This viewpoint is in marked contrast to the current perspective on some other chronic inflammatory epithelial disorders that afflict the skin, lungs, and gut, wherein host factors are believed to predispose to disease expression in the presence of ubiquitous environmental agents. Methods: The current review evaluates CRS etiology from this perspective and considers that CRS develops, in part, as an outcome of a dysfunctional host response. Specifically, evidence from our laboratory and others will be reviewed indicating that CRS is associated with a failure of the mechanical and immunologic barriers across the nasal mucosa. The hypothesis would further propose that genetic and epigenetic variation predisposes susceptible individuals to barrier failure in the presence of environmental stress leading to CRS. Results: From this unifying perspective, bacteria and fungi are seen as disease modifiers rather than primary etiologic agents. Conclusion: The goal is to place concepts of CRS pathophysiology in a framework consistent with a current understanding of chronic inflammation in general and epithelial disease in particular.
KW - Adaptive immune system
KW - Chronic rhinosinusitis
KW - Fungal hypothesis
KW - Immune barrier hypothesis
KW - Innate immunesystem
KW - Nasal polyps
KW - Superantigen hypothesis
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U2 - 10.2500/ajr.2008.22.3228
DO - 10.2500/ajr.2008.22.3228
M3 - Review article
C2 - 18786300
AN - SCOPUS:59949084049
SN - 1050-6586
VL - 22
SP - 549
EP - 559
JO - American Journal of Rhinology
JF - American Journal of Rhinology
IS - 6
ER -