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.

Highlights

  • Asthma is a common chronic inflammatory disease in the respiratory tract characterized by variable/ recurring symptoms of reversible airflow obstruction and bronchospasm [1]

  • The role of BEA in inhibiting inflammation was previously reported in CD-1 mice [7, 8]

  • It was reported that the proliferation of lymphocytes could be induced by PMA [11], and PMAinduced lymphocytic proliferation could be inhibited by Cyclosporine A (CsA) [12]

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Summary

Introduction

Asthma is a common chronic inflammatory disease in the respiratory tract characterized by variable/ recurring symptoms of reversible airflow obstruction and bronchospasm [1]. It is caused by a combination of genetic and environmental factors [2]. The inflammaroty cells such as lymphocytes, macrophages and neutrophils are involved in the pathogenesis of asthma. Components of the immune system mediators including cytokines, chemokines, histamine and leukotrienes are contributing factors of asthma [3]. The incidence of asthma has increased greatly since the 1970s. In 2011, it was diagnosed in 235-300 million people [4, 5] and caused 250,000 deaths globally [5]

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