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精氨酸分解代谢移动元件在社区获得性耐甲氧西林金黄色葡萄球菌USA300菌株进化及致病性中的作用

Arginine Catabolic Mobile Element in Evolution and Pathogenicity of the Community-Associated Methicillin-Resistant Strain USA300.

作者信息

Wu Kaiyu, Conly John, McClure Jo-Ann, Kurwa Habib A, Zhang Kunyan

机构信息

Department of Pathology & Laboratory Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada.

Department of Microbiology, Immunology & Infectious Diseases, University of Calgary, Calgary, Alberta T2N 4N1, Canada.

出版信息

Microorganisms. 2020 Feb 18;8(2):275. doi: 10.3390/microorganisms8020275.

Abstract

USA300 is a predominant community-associated methicillin-resistant strain which carries an arginine catabolic mobile element (ACME). ACME contains potential virulence factors including an arginine deiminase () pathway and an oligopeptide permease () system, which are proposed to play a role in bacterial virulence and transmission. However, the role of ACME in evolution and pathogenicity of USA300 remains to be elucidated. ACME and deletion mutants were created by allelic replacement from a USA300 clinical isolate. By comparing wild type and isogenic ACME deletion USA300 strains, ACME was shown not to contribute to bacterial survival on plastic surfaces, and mouse skin surfaces. ACME did not contribute to bacterial virulence in cell invasion and cytotoxicity assays, invertebrate killing assays and a mouse skin infection model. Wild-type ACME negative USA300 clinical isolates showed similar associations with invasive anatomic sites as ACME positive isolates. Our experiments also demonstrated that ACME can spontaneously excise from the bacterial chromosome to generate an ACME deletion strain at a low frequency. Our results do not support that the ACME element alone is a significant factor in the transmission and virulence of USA300 strain, and ACME may have been coincidently incorporated into the genome of USA300.

摘要

USA300是一种主要的社区相关性耐甲氧西林菌株,它携带一种精氨酸分解代谢移动元件(ACME)。ACME包含潜在的毒力因子,包括精氨酸脱亚氨酶()途径和寡肽通透酶()系统,这些被认为在细菌毒力和传播中发挥作用。然而,ACME在USA300进化和致病性中的作用仍有待阐明。通过从USA300临床分离株进行等位基因替换创建了ACME和缺失突变体。通过比较野生型和同基因ACME缺失的USA300菌株,发现ACME对细菌在塑料表面和小鼠皮肤表面的存活没有贡献。在细胞侵袭和细胞毒性试验、无脊椎动物杀伤试验以及小鼠皮肤感染模型中,ACME对细菌毒力没有贡献。野生型ACME阴性的USA300临床分离株与ACME阳性分离株在侵袭性解剖部位的关联相似。我们的实验还表明,ACME可以从细菌染色体上自发切除,以低频率产生ACME缺失菌株。我们的结果不支持ACME元件单独是USA300菌株传播和毒力的重要因素,并且ACME可能是偶然整合到USA300基因组中的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/793e/7074830/f7c7dc930d98/microorganisms-08-00275-g001.jpg

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