Current opinion in allergy and clinical immunology · 2013
Role of interleukin-32 in chronic rhinosinusitis.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАОбзорНазвание и аннотация: Перевод пока не подготовлен
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Keswani Anjeni, Kern Robert C, Schleimer Robert P, Kato Atsushi
Аннотация
PURPOSE OF REVIEW: IL-32 is a recently described proinflammatory cytokine and has been reported to be involved in inflammatory diseases. The purpose of this review is to discuss the role of IL-32 in chronic rhinosinusitis (CRS).
RECENT FINDINGS: Two groups have recently reported data regarding the expression of IL-32 in CRS. IL-32 was induced by IFN-γ, TNF-α, dsRNA, and incubation with Th1 cells in primary nasal epithelial cells. IL-32 may be elevated in epithelial cells from patients with CRS without nasal polyps. IL-32 was significantly elevated in whole sinonasal tissue samples of nasal polyps compared with control tissue. IL-32 mRNA expression positively correlated with mRNA for CD3 and macrophage mannose receptor in nasal polyp tissue. Immunohistochemical studies demonstrated localization of IL-32 in epithelium, CD3(+) and CD68(+) cells, suggesting that epithelial cells, T cells, and macrophages are the major IL-32-producing cells in CRS. Activation of these cell types may trigger IL-32-related inflammation in CRS.
SUMMARY: Elevated levels of IL-32 may play a role in the pathogenesis of CRS through its role as a proinflammatory cytokine and as an endogenous enhancer of pathogen-dependent cytokine production.
RECENT FINDINGS: Two groups have recently reported data regarding the expression of IL-32 in CRS. IL-32 was induced by IFN-γ, TNF-α, dsRNA, and incubation with Th1 cells in primary nasal epithelial cells. IL-32 may be elevated in epithelial cells from patients with CRS without nasal polyps. IL-32 was significantly elevated in whole sinonasal tissue samples of nasal polyps compared with control tissue. IL-32 mRNA expression positively correlated with mRNA for CD3 and macrophage mannose receptor in nasal polyp tissue. Immunohistochemical studies demonstrated localization of IL-32 in epithelium, CD3(+) and CD68(+) cells, suggesting that epithelial cells, T cells, and macrophages are the major IL-32-producing cells in CRS. Activation of these cell types may trigger IL-32-related inflammation in CRS.
SUMMARY: Elevated levels of IL-32 may play a role in the pathogenesis of CRS through its role as a proinflammatory cytokine and as an endogenous enhancer of pathogen-dependent cytokine production.