title: Interleukin-32γ suppresses allergic airway inflammation in mouse models of asthma.
abstract: Asthma is a chronic airway inflammatory disease typically associated with T helper cell type 2 (Th2) cytokines. IL-32, first reported as an inducer of tumor necrosis factor (TNF)-α, is an inflammatory cytokine involved in various autoinflammatory diseases, viral infection, and cancer-related inflammation. However, the role of IL-32γ in asthma has not been clearly elucidated. In this study, the levels of IL-32γ in sputum from patients with asthma were measured by ELISA, and IL-32γ function was investigated in murine models of asthma with human IL-32γ-overexpressed transgenic (IL-32γ TG) mice. The therapeutic effect of recombinant IL-32γ (rIL-32γ) on allergic inflammation was also evaluated through bronchoalveolar lavage fluid analysis and histopathologic examinations. Sputum IL-32γ levels from patients with asthma were lower than those from healthy control subjects. In an acute mouse model of asthma, IL-32γ TG mice exhibited significantly reduced airway inflammation compared with that in wild-type mice. The production of Th1 cytokines, such as TNF-α and IFN-γ, and Th2 cytokines, such as IL-4, IL-5, and IL-13, was decreased in the lungs of IL-32γTG mice. On the contrary, the expression of IL-10 and IL-10-producing CD11b(+) monocytic cells was significantly increased in the lungs of ovalbumin-sensitized IL-32γ TG mice. In addition, rIL-32γ treatment revealed a suppressive effect on the airway inflammation in a chronic mouse model of asthma. The results of this study suggest that IL-32γ may have a preventive role in the development of allergic airway inflammation and could be a potential novel therapeutic target for bronchial asthma.
authors: 1 Asan Institute for Life Science, Seoul, Korea.
authors: Bo-Ram
authors: BR
authors: Bang
authors: Hyouk-Soo
authors: HS
authors: Kwon
authors: Soo-Hyun
authors: SH
authors: Kim
authors: Sun-Young
authors: SY
authors: Yoon
authors: Ji-Da
authors: JD
authors: Choi
authors: Gyong Hwa
authors: GH
authors: Hong
authors: Sunjoo
authors: S
authors: Park
authors: Tae-Bum
authors: TB
authors: Kim
authors: Hee-Bom
authors: HB
authors: Moon
authors: You Sook
authors: YS
authors: Cho
mesh_terms: D000818:Animals; D001249:Asthma / Q000276:immunology*; D001980:Bronchi / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D004195:Disease Models, Animal; D004804:Eosinophils / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000276:immunology*; D007371:Interferon-gamma / Q000276:immunology; D007378:Interleukins / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; C569037:interleukin-32, mouse; D007371:Interferon-gamma; D010047:Ovalbumin