| First Author | Bang BR | Year | 2014 |
| Journal | Am J Respir Cell Mol Biol | Volume | 50 |
| Issue | 6 | Pages | 1021-30 |
| PubMed ID | 24328857 | Mgi Jnum | J:232080 |
| Mgi Id | MGI:5775880 | Doi | 10.1165/rcmb.2013-0234OC |
| Citation | Bang BR, et al. (2014) Interleukin-32gamma suppresses allergic airway inflammation in mouse models of asthma. Am J Respir Cell Mol Biol 50(6):1021-30 |
| abstractText | 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)-alpha, is an inflammatory cytokine involved in various autoinflammatory diseases, viral infection, and cancer-related inflammation. However, the role of IL-32gamma in asthma has not been clearly elucidated. In this study, the levels of IL-32gamma in sputum from patients with asthma were measured by ELISA, and IL-32gamma function was investigated in murine models of asthma with human IL-32gamma-overexpressed transgenic (IL-32gamma TG) mice. The therapeutic effect of recombinant IL-32gamma (rIL-32gamma) on allergic inflammation was also evaluated through bronchoalveolar lavage fluid analysis and histopathologic examinations. Sputum IL-32gamma levels from patients with asthma were lower than those from healthy control subjects. In an acute mouse model of asthma, IL-32gamma TG mice exhibited significantly reduced airway inflammation compared with that in wild-type mice. The production of Th1 cytokines, such as TNF-alpha and IFN-gamma, and Th2 cytokines, such as IL-4, IL-5, and IL-13, was decreased in the lungs of IL-32gammaTG 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-32gamma TG mice. In addition, rIL-32gamma treatment revealed a suppressive effect on the airway inflammation in a chronic mouse model of asthma. The results of this study suggest that IL-32gamma may have a preventive role in the development of allergic airway inflammation and could be a potential novel therapeutic target for bronchial asthma. |
