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周期抑制因子与人类神经元细胞的侵袭有关。

Cycle-Inhibiting Factor Is Associated with Invasion in Human Neuronal Cells.

作者信息

Rungruengkitkun Amporn, Jitprasutwit Niramol, Muangkaew Watcharamat, Suttikornchai Chantira, Tandhavanant Sarunporn, Indrawattana Nitaya, Ampawong Sumate, Sukphopetch Passanesh, Chantratita Narisara, Pumirat Pornpan

机构信息

Department of Microbiology and Immunology, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand.

Center for Vaccine Development, Institute of Molecular Biosciences, Mahidol University, Nakhon Pathom 73170, Thailand.

出版信息

Biology (Basel). 2022 Oct 1;11(10):1439. doi: 10.3390/biology11101439.

Abstract

Burkholderia pseudomallei is a pathogenic bacterium that causes human melioidosis, which is associated with a high mortality rate. However, the underlying mechanisms of B. pseudomallei pathogenesis are largely unknown. In this study, we examined the infection of human neuronal SH-Sy5y cells by several clinically relevant B. pseudomallei strains. We found that all tested B. pseudomallei strains can invade SH-Sy5y cells, undergo intracellular replication, cause actin-tail formation, and form multinucleated giant cells. Additionally, a deletion mutant of B. pseudomallei cycle-inhibiting factor (cif) was constructed that exhibited reduced invasion in SH-Sy5y cells. Complementation of cif restored invasion of the B. pseudomallei cif-deleted mutant. Our findings enhance understanding of B. pseudomallei pathogenicity in terms of the virulence factor Cif and demonstrate the function of Cif in neurological melioidosis. This may eventually lead to the discovery of novel targets for treatment and a strategy to control the disease.

摘要

类鼻疽伯克霍尔德菌是一种可导致人类类鼻疽的致病细菌,该病死亡率很高。然而,类鼻疽伯克霍尔德菌致病的潜在机制在很大程度上尚不清楚。在本研究中,我们检测了几种临床相关的类鼻疽伯克霍尔德菌菌株对人神经元SH-Sy5y细胞的感染情况。我们发现,所有测试的类鼻疽伯克霍尔德菌菌株均可侵入SH-Sy5y细胞,在细胞内复制,导致肌动蛋白尾形成,并形成多核巨细胞。此外,构建了类鼻疽伯克霍尔德菌周期抑制因子(cif)的缺失突变体,该突变体在SH-Sy5y细胞中的侵袭能力降低。cif的互补恢复了类鼻疽伯克霍尔德菌cif缺失突变体的侵袭能力。我们的研究结果从毒力因子Cif方面增强了对类鼻疽伯克霍尔德菌致病性的理解,并证明了Cif在神经类鼻疽中的作用。这最终可能会导致发现新的治疗靶点和控制该疾病的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5f9/9598235/3f3969c25a8e/biology-11-01439-g001.jpg

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