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.
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-32in 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.
Authors: P Felaco; M L Castellani; M A De Lutiis; M Felaco; F Pandolfi; V Salini; D De Amicis; J Vecchiet; S Tete; C Ciampoli; F Conti; G Cerulli; A Caraffa; P Antinolfi; C Cuccurullo; A Perrella; T C Theoharides; P Conti; E Toniato; D Kempuraj; Y B Shaik Journal: J Biol Regul Homeost Agents Date: 2009 Jul-Sep Impact factor: 1.711
Authors: J H Oh; M-C Cho; J-H Kim; S Y Lee; H J Kim; E S Park; J O Ban; J-W Kang; D-H Lee; J-H Shim; S B Han; D C Moon; Y H Park; D-Y Yu; J-M Kim; S H Kim; D-Y Yoon; J T Hong Journal: Oncogene Date: 2011-03-21 Impact factor: 9.867
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