Figure 5.
Heterogeneity of chronic rhinosinusitis (CRS). According to this model, variations in the expression of genes that govern critical host epithelial pathways may increase the susceptibility to CRS. Environmental factors, rather than discrete etiologic agents, can be seen as disease modifiers that skew the clinical presentation in an individual patient. Fungi may accentuate both T-helper type 1 (TH1) and TH2 cytokine expression. Chronic inflammatory disorders occur at other sites of interface with the outside world, including the skin, gut, and lungs. (Illustration by William E. Walsh, MD, CMI, 2008 William Walsh; used with permission.)