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铜绿假单胞菌的合并感染会影响金黄色葡萄球菌的毒力,并加剧感染的严重程度。

Co-infection with Pseudomonas aeruginosa impacts virulence of Staphylococcus aureus and intensifies the severity of infection.

机构信息

Department of Bioscience, Barrett Hodgson University, Karachi, Pakistan.

Department of Biotechnology, Dalian Medical University, Dalian, PR China.

出版信息

Pak J Pharm Sci. 2020 Sep;33(5):1933-1937.

Abstract

Multi-specie infections display diverse interactions among pathogens that influence the severity of disease. Staphylococcus aureus and Pseudomonas aeruginosa are the two most important opportunistic, nosocomial and drug-resistant pathogens. Poly-infections due to S. aureus and P. aeruginosa are more destructive and result in worse patient outcome than mono-infection. The two organisms are commonly isolated from cystic fibrosis respiratory cultures. Studies demonstrated that S. aureus pre-colonization among cystic fibrosis patients is a hazardous for beginning P. aeruginosa aviation route infection. This work meant to explore the impact of P. aeruginosa on the destructiveness of S. aureus and the level of disease's seriousness by utilizing in-vitro co-culture and host cell model. The outcomes showed that P. aeruginosa outcompetes and suppresses the growth of S. aureus when co-cultured. The host factors expression profile indicated elevated expression of TNFα, IL-6 and IL-12, recommending the unique mechanism of host cell healing inhibition by multispecies. Co-infection resulted in significant increase in IL-8 together with the 10-fold induction of iNOS expression when contrast with S. aureus mono-infection. This indicates that the presence of P. aeruginosa heads the infection towards more severity and complications and delays cell healing process.

摘要

多物种感染表现出病原体之间的多种相互作用,影响疾病的严重程度。金黄色葡萄球菌和铜绿假单胞菌是两种最重要的机会性、医院获得性和耐药病原体。金黄色葡萄球菌和铜绿假单胞菌引起的混合感染比单一感染更具破坏性,导致患者预后更差。这两种生物通常从囊性纤维化呼吸道培养物中分离出来。研究表明,囊性纤维化患者中金黄色葡萄球菌的定植前是开始铜绿假单胞菌航空途径感染的危险。这项工作旨在通过体外共培养和宿主细胞模型来探索铜绿假单胞菌对金黄色葡萄球菌的破坏性和疾病严重程度的影响。结果表明,当共培养时,铜绿假单胞菌会与金黄色葡萄球菌竞争并抑制其生长。宿主因子表达谱表明 TNFα、IL-6 和 IL-12 的表达水平升高,表明多物种抑制宿主细胞愈合的独特机制。与金黄色葡萄球菌单一感染相比,共感染导致 IL-8 的显著增加,同时诱导 iNOS 表达增加 10 倍。这表明铜绿假单胞菌的存在使感染变得更加严重和复杂,并延迟细胞愈合过程。

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