title: Adenovirus-mediated interleukin-35 gene transfer suppresses allergic airway inflammation in a murine model of asthma.
abstract: OBJECTIVE
  Asthma is thought to result from the generation of T helper type 2 (Th2) responses, leading to bronchial inflammation. Interleukin (IL)-35 is a recently described member of IL-12 cytokine family that plays a critical role in influencing Th cell differentiation and inflammatory processes. The aim of this study was to examine the effect of adenovirus expressing IL-35 (AdIL-35) on allergic airway hyperresponsiveness (AHR) and inflammation in a mouse model of asthma.
  
  
  METHODS
  BALB/c mice were subjected to an established model of allergic airway disease. AdIL-35 was administered intranasally and the effect of IL-35 on Th2 responses, pulmonary inflammation, goblet cell metaplasia, and AHR were assessed.
  
  
  RESULTS
  Transfer of AdIL-35 significantly reduced the severity of AHR and numbers of inflammatory cells and levels of IL-4, IL-5, IL-13, and IL-17 in bronchoalveolar lavage fluid, compared with administration of a control virus. Moreover, AdIL-35 elevated the numbers of CD4+CD25+Foxp3+ regulatory T cells in the lungs. Histological analysis showed that AdIL-35 inhibited allergic lung tissue inflammation and mucus hypersecretion.
  
  
  CONCLUSIONS
  These results demonstrate that adenovirus-mediated delivery of interleukin-35 gene can mitigate allergic airway inflammation in experimental asthma and suggest that IL-35 may offer a novel therapeutic approach to treat allergic asthma.
authors: Department of Immunology, Ningbo University School of Medicine, 818 Fenghua Road, Jiangbei District, Ningbo, 315211, China.
authors: Yan
authors: Y
authors: Li
authors: Department of Immunology, Ningbo University School of Medicine, 818 Fenghua Road, Jiangbei District, Ningbo, 315211, China.
authors: Xiuhe
authors: X
authors: Pan
authors: Department of Immunology, Ningbo University School of Medicine, 818 Fenghua Road, Jiangbei District, Ningbo, 315211, China.
authors: Xiao
authors: X
authors: Peng
authors: Department of Histology and Embryology, College of Basic Medicine, Beihua University, Jilin, 132013, China. hzrlsb@sina.com.
authors: Shubo
authors: S
authors: Li
authors: Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, 515041, China.
authors: Yanchun
authors: Y
authors: Zhou
authors: Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, 515041, China.
authors: Xiaoxuan
authors: X
authors: Zheng
authors: Department of Immunology, Ningbo University School of Medicine, 818 Fenghua Road, Jiangbei District, Ningbo, 315211, China. limingcai@nbu.edu.cn.|Institute of Inflammation and Immune Diseases, Shantou University Medical College, Shantou, 515041, China. limingcai@nbu.edu.cn.
authors: Mingcai
authors: M
authors: Li
mesh_terms: D000256:Adenoviridae / Q000235:genetics*; D000281:Administration, Intranasal; D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D016535:Bronchial Hyperreactivity / Q000188:drug therapy*; D001992:Bronchoalveolar Lavage Fluid; D005260:Female; D018014:Gene Transfer Techniques; D020397:Goblet Cells / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy*; D007378:Interleukins / Q000096:biosynthesis / Q000235:genetics*; D051379:Mice; D008807:Mice, Inbred BALB C; D011014:Pneumonia / Q000188:drug therapy / Q000473:pathology; D012137:Respiratory System; D018418:Th2 Cells / Q000187:drug effects
chemical_list: D018927:Anti-Asthmatic Agents; D007378:Interleukins; C569375:interleukin-35, mouse
keywords: Airway inflammation; Allergic asthma; Eosinophils; Hyperresponsiveness; IL-35; Regulatory T cells; Th17 cells