Current opinion in otolaryngology & head and neck surgery · 2008
The role of cytokines in chronic rhinosinusitis with nasal polyps.
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Otto Bradley A, Wenzel Sally E
Аннотация
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 Th2-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, Th2 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 antagonistic roles to Th2 inflammation and both are downregulated in nasal polyps. Tumor necrosis factor-alpha 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.
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, Th2 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 antagonistic roles to Th2 inflammation and both are downregulated in nasal polyps. Tumor necrosis factor-alpha 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.