Oncotarget

Research Papers: Pathology:

Beauveria attenuates asthma by inhibiting inflammatory response and inducing lymphocytic cell apoptosis

Jingying Zhang, Xianmei Zhou and Jiping Zhu _

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Oncotarget. 2016; 7:74557-74568. https://doi.org/10.18632/oncotarget.12958

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Abstract

Jingying Zhang1, Xianmei Zhou1 and Jiping Zhu1

1 Department of Respiratory Medicine, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, China

Correspondence to:

Jiping Zhu, email:

Keywords: asthma, beauveria, inflammation, lymphocytes, cell apoptosis, Pathology Section

Received: July 20, 2016 Accepted: October 14, 2016 Published: October 27, 2016

Abstract

The present study aimed to investigate the role of beauveria (BEA) in asthma. We investigated the cytotoxic effect of BEA on the proliferation of inflammatory cells and secretion of inflammatory mediators both in-vitro and in-vivo. In in-vitro studies, BEA inhibited lymphocytic cell proliferation and the proliferation of lymphocytic cells induced by Phorbol-12-myristate-13-acetate (PMA). We used ELISA to test the effects of BEA on the secretion of inflammatory factors including tumor necrosis factor-alpha (TNF-α), interleukin-12 (IL-12) and interferon-gamma (IFN-γ). Flow cytometry was used to evaluate the influence of BEA on cell apoptosis. The effect of BEA on the cell numbers of eosinophils, lymphocytes, macrophages, neutrophils and other cells in mouse bronchoalveolar lavage fluid (BALF) was also evaluated. The expression of apoptosis related molecules Bax, Caspase-3 and Bcl-2 was examined by Western blotting analysis. Our results indicated that BEA played a protective role in asthma. BEA inhibited lymphocytic cell proliferation and secretion of inflammatory mediators. BEA promoted cell apoptosis, stimulated the expression of Bax and Caspase-3 and inhibited Bcl-2 protein expression in a dose-dependent manner. In in-vivo experiments, BEA reduced the cell number of eosinophils, lymphocytes, macrophages, neutrophils and other cells in mouse BALF. BEA inhibited secretion of inflammatory mediators, stimulated expression of Bax and Caspase-3, and inhibited expression of Bcl-2 in mouse lung tissue dose-dependently. All together, our results indicated that BEA could attenuate asthma by inhibiting inflammatory response and induce apoptosis of inflammatory cells.


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