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Tian B.-P.,Zhejiang University | Tian B.-P.,Key Site of National Clinical Research Center for Respiratory Disease | Hua W.,Zhejiang University | Hua W.,Key Site of National Clinical Research Center for Respiratory Disease | And 17 more authors.
American Journal of Respiratory Cell and Molecular Biology | Year: 2015

IL-17 is known to play important roles in immune and inflammatory disease, such as in asthma, but its functions in allergic airway inflammation are still controversial, and the molecular mechanisms mediating these functions remain unclear. Increased production of eosinophils in bone marrow and their emergence in the airway have been linked to the onset and progression of allergic asthma. In this study, we investigated the effects of exogenous IL-17 on allergic airway inflammation and explored the underlying molecular mechanisms through eosinophil generation. Exogenous IL-17 significantly attenuated the features of allergic inflammation induced by ovalbumin in mice. It inhibited eosinophil differentiation both in vivo and in vitro, accompanied by down-regulated expression of CC chemokine receptor 3, GATA binding protein 1 (GATA-1), and GATA binding protein 2 (GATA-2), as well as reduced formation of commonmyeloid progenitors and eosinophil progenitors, butwithout influencing eosinophil apoptosis. IL-17 also significantly decreased the number of eosinophils in IL-5-transgenic mice, although it notably increased the levels of IL-3, IL-5, and granulocyte/macrophage colony-stimulating factor. In addition, IL-17 had little effect on secretion of the inflammatory cytokines by eosinophils.Neutralization of endogenous IL-17 significantly augmented eosinophil recruitment in the airways. Together, these findings suggest that exogenous IL-17 protects against allergic airway inflammation, most likely through inhibition of the eosinophil differentiation in bone marrow. © 2015 by the American Thoracic Society. Source


Tian B.-P.,Zhejiang University | Tian B.-P.,Key Site of National Clinical Research Center for Respiratory Disease | Zhou H.-B.,Zhejiang University | Zhou H.-B.,Key Site of National Clinical Research Center for Respiratory Disease | And 7 more authors.
Microbes and Infection | Year: 2014

Allergic diseases result from over-reaction of the immune system in response to exogenous allergens, where inflammatory cells have constantly extended longevity and contribute to an on-going immune response in allergic tissues. Here, we review disequilibrium in the death and survival of epithelial cells and inflammatory cells in the pathological processes of asthma, atopic dermatitis, and other allergic diseases. © 2014 Published by Elsevier Masson SAS on behalf of Institut Pasteur. Source

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