The role of cytokines in chronic rhinosinusitis with nasal polyps

Purpose of review This article reviews the recent literature regarding select cytokines involved in chronic rhinosinusitis with nasal polyps. Chronic rhinosinusitis with nasal polyps is generally characterized by eosinophilic infiltration and a T(h)2-biased cytokine profile. However, the mechanisms that lead to nasal polyps are not clear. Recent findings There has been a significant amount of work identifying cytokines that are either upregulated or downregulated in chronic rhinosinusitis with nasal polyps. In general, T(h)2 cytokines such as IL-4 and IL-5 are upregulated. IL-4 promoter polymorphisms are associated with nasal polyps, and IL-4 appears to potentiate the immune response of fibroblasts. IL-5 release from nasal polyps is induced by Staph enterotoxin B and upregulation may be localized to nasal polyps. IL-8 appears to be upregulated by Staphylococcus epidermidis and may modulate remodeling in nasal polyps. Interferon-gamma and transforming growth factor-beta have antagonsitic roles to T(h)2 inflammation and both are downregulated in nasal polyps. Tumor necrosis factor-a and IL-1 are pro-inflammatory cytokines that are upregulated in nasal polyps. Single nucleotide polymorphisms for both cytokines have been identified in nasal polyps. Summary Several studies have reported on various cytokines that correlate to the chronic rhinosinusitis with nasal polyps phenotype; however, more insight into the mechanisms that lead to altered cytokine profiles and the nasal polyps phenotype is needed.