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后续感染通过阻断肠道细胞增殖,对秀丽隐杆线虫的蛋白质组产生不同影响。

Subsequent infection differentially affects the proteome of Caenorhabditis elegans by abrogating the intestinal cell proliferation.

机构信息

Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, 630 003, Tamil Nadu, India.

Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, 630 003, Tamil Nadu, India.

出版信息

Microb Pathog. 2022 Jan;162:105350. doi: 10.1016/j.micpath.2021.105350. Epub 2021 Dec 21.

DOI:10.1016/j.micpath.2021.105350
PMID:34952153
Abstract

With a wide range of bacterial infections growing, it has become a big challenge to the research field to combat the newly emerging diseases. Immuno-compromised patients are vulnerable to opportunistic infections. P. mirabilis, an opportunistic pathogen infects the nematode when the immune system is compromised. In the present study, the C. elegans was pre-exposed to S. aureus for a short term, and then consecutively infected with P. mirabilis. The primary infection caused by S. aureus makes the immune system of C. elegans vulnerable making it easy for P. mirabilis to colonize efficiently during subsequent exposure, thereby stimulating the immune system of the nematode. In this study, the C. elegans exposed to the pathogens (S. aureus 4 h/P. mirabilis 40 h and S. aureus 8 h/P. mirabilis 60 h time points) showed a substantial difference in the banding patterns of SDS-PAGE gel, when compared to their respective OP50 fed controls. 2-DE identified a total of 235 proteins from all the time points which had >2 fold regulation. The regulated protein spots were identified by MALDI-ToF/ToF analysis and one common protein CDC-25.1 was found to be regulated in all the comparative time points. CDC-25.1 seemed to down regulate during subsequent infection and up regulate in single infection. The transcriptomic regulation of cdc-25.1 also reflects the protein regulation. In addition to it, survival assay in cdc-25.1 mutant nematodes confirm the susceptibility of host during subsequent infection.

摘要

随着越来越多的细菌感染的出现,对抗新出现的疾病已成为研究领域的一大挑战。免疫功能低下的患者容易受到机会性感染。当免疫系统受损时,机会性病原体奇异变形杆菌会感染线虫。在本研究中,先用金黄色葡萄球菌短期预感染秀丽隐杆线虫,然后再连续感染奇异变形杆菌。金黄色葡萄球菌引起的原发性感染使秀丽隐杆线虫的免疫系统变得脆弱,使奇异变形杆菌在后一次暴露时能够有效地定植,从而刺激线虫的免疫系统。在这项研究中,与各自的 OP50 喂养对照组相比,暴露于病原体(金黄色葡萄球菌 4 小时/奇异变形杆菌 40 小时和金黄色葡萄球菌 8 小时/奇异变形杆菌 60 小时时间点)的秀丽隐杆线虫的 SDS-PAGE 凝胶的条带模式显示出显著差异。2-DE 从所有时间点总共鉴定出 235 种蛋白,其调控倍数>2。通过 MALDI-ToF/ToF 分析鉴定出受调控的蛋白斑点,发现一个共同的蛋白 CDC-25.1 在所有比较时间点都受到调控。CDC-25.1 在随后的感染中似乎下调,而在单次感染中上调。cdc-25.1 的转录组调控也反映了蛋白调控。除此之外,cdc-25.1 突变线虫的存活实验证实了宿主在后一次感染中的易感性。

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