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Abstract: Interleukin (IL)-33 is a recently described member of the IL-1 family and has been shown to induce production of T helper type 2 cytokines. In this study, an anti-IL-33 antibody was evaluated against pulmonary inflammation in mice sensitized and challenged with ovalbumin. The anti-IL-33 or a control antibody (150μg/mouse) was given intraperitoneally as five doses before the sensitization and antigen challenge. Treatment with anti-IL-33 significantly reduced serum IgE secretion, the numbers of eosinophils and lymphocytes, and concentrations of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid compared with administration of a control antibody. Histological examination of lung tissue demonstrated that anti-IL-33 significantly inhibited allergen-induced lung eosinophilic inflammation and mucus hypersecretion. Our data demonstrate for the first time that anti-IL-33 antibody can prevent the development of asthma in a mouse model and indicate that blockade of IL-33 may be a new therapeutic strategy for allergic asthma. [Copyright &y& Elsevier]

Abstract Obesity is associated with a chronic inflammatory response. Interleukin (IL)-38 is a poorly characterized cytokine of the IL-1 family with anti-inflammatory activity. The role of IL-38 in obesity-induced inflammation and insulin resistance remains unknown. In this study, we investigated the effects of IL-38 expression by hydrodynamic-based gene delivery on high-fat diet-induced obesity in mice. Transfer of plasmid DNA encoding IL-38 reduced weight gain, liver fat content, adipose tissue weight, and obesity-induced insulin resistance compared with administration of a control plasmid. Moreover, IL-38 gene delivery inhibited the production of inflammatory mediators including IL-1β, IL-6, and monocyte chemotactic protein-1. These results suggest that IL-38 is a potential new target for the treatment of obesity. Highlights • IL-38 inhibits HFD-induced obesity. • IL-38 reduces HFD-induced systemic insulin resistance. • IL-38 inhibits HFD-induced hepatic fat accumulation and liver damage. • IL-38 inhibits HFD induced-hypertrophy in adipocytes. • IL-38 suppresses HFD-induced inflammatory cytokines production. [ABSTRACT FROM AUTHOR]

Highlights: [•] IL-28B impairs cigarette smoke-induced lung inflammation. [•] IL-28B inhibits cigarette smoke-elicited lymphocyte, neutrophil and macrophage infiltration in the lung. [•] IL-28B decreases expression of cigarette smoke-induced inflammatory mediators. [ABSTRACT FROM AUTHOR]