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2016 ; 7
(46
): 74557-74568
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Beauveria attenuates asthma by inhibiting inflammatory response and inducing
lymphocytic cell apoptosis
#MMPMID27801673
Zhang J
; Zhou X
; Zhu J
Oncotarget
2016[Nov]; 7
(46
): 74557-74568
PMID27801673
show ga
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-?), interleukin-12 (IL-12) and
interferon-gamma (IFN-?). 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.