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细胞内杆菌肺炎在流感A共感染期间发展出增强的化诺持久性

Mirelys Hernandez-Morfa^1,2, Nicolas M Reinoso-Vizcaino^1,2, Victoria E Zappia^1,2

¹Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI)-Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Córdoba, Argentina.

Frontiers in microbiology

|July 22, 2024

概括

流感A病毒感染通过促进宿主细胞内诺基诺的持久性来增强Streptococcus pneumoniae的存活率. 这是由于氧化应激增加和自功能受损而引起的,这凸显了治疗共感染的挑战.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

* *肺炎链球菌*会导致严重的并发症,特别是在感染甲型流感病毒 (IAV) 后.
* IAV感染增加了S.肺炎的细胞内存活率,并促进诺基诺 (FQ) 持久性.
*细胞内FQ持久性是由宿主细胞氧化应激引发的,使细菌能够在高度药物下生存.

研究的目的:

* 调查IAV感染如何影响肺炎球菌细胞内FQ持久性.
* 确定导致这种增强持久性的宿主和细菌因素.

主要方法:

* 在感染了IAV的人类细胞 (肺细胞,巨细胞,中性粒细胞) 中研究了S. pneumoniae*生存率和FQ持久性.
* 评估了受感染细胞中的氧化应激水平和自功能 (自-溶融合).
通过基因选,确定了参与氧化应激反应的S. pneumoniae基因.

主要成果:

* IAV感染显著增强了感染肺细胞,巨细胞和中性粒细胞中的肺炎球菌FQ持久性.
* IAV感染细胞中氧化应激增加有助于增强FQ持久性.
*这种表型在具有自能力的细胞中更为明显,这表明IAV诱导的自阻塞起着作用.
*发现几个*S. pneumoniae*氧化应激反应基因 (*sodA*, *clpL*, *nrdH*, *psaB*) 对于FQ持续性至关重要.

结论:

* IAV感染创造了一个促进 * S. pneumoniae * 诺基诺持续性的细胞环境.
* 这种机制涉及氧化应激增加和潜在的自功能受损.
* 介导氧化应激反应的特定细菌基因对于这种抗生素耐药性至关重要.
*研究结果强调在治疗流感患者肺炎球菌感染时需要考虑病毒与宿主相互作用.

关键词:

肺炎链球菌的肺炎链球菌.自自是自的过程.诺基诺的化.甲型流感是一类流感.细胞内生存率细胞内生存率氧化应激是一种氧化应激.持续性持久性压力反应应对压力的反应.

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