کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8749807 | 1593674 | 2018 | 25 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Epigallocatechin gallate can attenuate human alveolar epithelial cell injury induced by alpha-haemolysin
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
ایمنی شناسی و میکروب شناسی
میکروب شناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Epigallocatechin gallate can attenuate human alveolar epithelial cell injury induced by alpha-haemolysin Epigallocatechin gallate can attenuate human alveolar epithelial cell injury induced by alpha-haemolysin](/preview/png/8749807.png)
چکیده انگلیسی
Staphylococcus aureus (S. aureus) is a common cause of hospital-acquired infection and has become an epidemic globally. Alpha-haemolysin (α-haemolysin), a pore-forming toxin, is one of the most important virulence factors secreted by most S. aureus strains. α-haemolysin monomers form a 232.4-kDa membrane-inserted heptamer by self-assembling to cause host cell lysis and death. Consequently, α-haemolysin plays a significant role in the pathogenesis of S. aureus, and it could be the target for the treatment of staphylococcal infection. In this study, epigallocatechin gallate (EGCg), a natural compound with little anti-S. aureus activity, was shown to reduce the haemolytic activity of α-haemolysin by inhibiting the self-assembly of the heptamer. When EGCg was added into a co-cultured system of human alveolar epithelial (A549) cells and bacterial suspension, α-haemolysin-induced cell injury was significantly attenuated. These results indicate that EGCg could effectively reduce the cytotoxicity of the toxin by interacting with α-haemolysin. This study provides the basis for the development of anti-virulence drugs for the treatment of S. aureus infection.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbial Pathogenesis - Volume 115, February 2018, Pages 222-226
Journal: Microbial Pathogenesis - Volume 115, February 2018, Pages 222-226
نویسندگان
Yonglin Zhou, Chengzhen Chen, Juan Pan, Xuming Deng, Jianfeng Wang,