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自噬在炭疽致病性中的影响。

Implications of autophagy in anthrax pathogenicity.

作者信息

Tan Yian Kim, Vu Hao A, Kusuma Caroline M, Wu Aiguo

机构信息

DSO National Laboratories, Singapore, Singapore.

出版信息

Autophagy. 2009 Jul;5(5):734-5. doi: 10.4161/auto.5.5.8567. Epub 2009 Jul 30.

Abstract

The etiological agent for anthrax is Bacillus anthracis, which produces lethal toxin (LT) that exerts a myriad of effects on many immune cells. In our previous study, it was demonstrated that LT and protective antigen (PA) induce autophagy in mammalian cells. Preliminary results suggest that autophagy may function as a cellular defense mechanism against LT-mediated toxemia. This degradation pathway may also be relevant to other aspects of the immune response in both innate and adaptive immunity. Understanding the role of autophagy in response to anthrax infection and the possibility of modulating this degradation pathway as potential countermeasures are subjects for further investigation.

摘要

炭疽的病原体是炭疽芽孢杆菌,它产生的致死毒素(LT)会对许多免疫细胞产生多种影响。在我们之前的研究中,已证明LT和保护性抗原(PA)可诱导哺乳动物细胞发生自噬。初步结果表明,自噬可能作为一种细胞防御机制来抵御LT介导的毒血症。这种降解途径也可能与固有免疫和适应性免疫中免疫反应的其他方面相关。了解自噬在应对炭疽感染中的作用以及调节这种降解途径作为潜在对策的可能性,是有待进一步研究的课题。

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