2015 Fiscal Year Final Research Report
Mechanism of Clostridium perfringes beta-toxin-induced cytotoxicity
| Project/Area Number |
25460552
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Bacteriology (including mycology)
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| Research Institution | Tokushima Bunri University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | ウエルシュ菌β毒素 / THP-1細胞 / 細胞毒性 / p38MAPK |
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| Outline of Final Research Achievements |
Clostridium perfringens beta-toxin is an important agent of necrotic enteritis and enterotoxemia. Beta-toxin is a pore-forming toxin (PFT) that causes cytotoxicity. We investigate the role of the MAPK pathways in the toxic effect of beta-toxin. In THP-1 cells, beta-toxin formed oligomers on lipid rafts in membranes and induced the efflux of K(+) from THP-1 cells. The phosphorylation of p38 MAPK and JNK occurred in response to an attack by beta-toxin. p38 MAPKand JNK inhibitors enhanced toxin-induced cell death. Incubation in K(+)-free medium intensified p38 MAPK activation and cell death induced by the toxin, while incubation in K(+)-high medium prevented those effects. While streptolysin O (SLO) reportedly activates p38 MAPK via reactive oxygen species (ROS), we showed that this pathway did not play a major role in p38 phosphorylation in beta-toxin-treated cells. Therefore, we propose that beta-toxin induces activation of the MAPK pathway to promote host cell survival.
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| Free Research Field |
細菌学
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