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甲型流感病毒(H1N1)pd m09 和 H3N2 感染期间肺泡上皮细胞表面活性蛋白-C 和 CD74 表达降低。

Decreased expression of surfactant Protein-C and CD74 in alveolar epithelial cells during influenza virus A(H1N1)pdm09 and H3N2 infection.

机构信息

Instituto de Ciencia y Tecnología Dr. César Milstein, CONICET, Saladillo 2468, C1440FFX, Ciudad de Buenos Aires, Argentina; Instituto de Quimica Física de los Materiales, Medio Ambiente y Energía (INQUIMAE-CONICET). Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, 2160, Buenos Aires, Argentina.

Instituto Nacional de Enfermedades Infecciosas ANLIS "Dr. C. G. Malbrán", Buenos Aires, Argentina.

出版信息

Microb Pathog. 2023 Mar;176:106017. doi: 10.1016/j.micpath.2023.106017. Epub 2023 Feb 1.

Abstract

The primary replication site of Influenza A virus (IAV) is type II alveolar epithelial cells (AECII), which are central to normal lung function and present important immune functions. Surfactant components are synthesized primarily by AECII, which play a crucial role in host defense against infection. The aim of this study was to analyze if the impact of influenza infection is differential between A(H1N1)pdm09 and A/Victoria/3/75 (H3N2) on costimulatory molecules and ProSP-C expression in AECII from BALB/c mice infected and A549 cell line infected with both strains. Pandemic A(H1N1)pdm09 and A/Victoria/3/75 (H3N2) were used to infect BALB/c mice and the A549 cell line. We evaluated the surface expression of co-stimulatory molecules (CD45/CD31/CD74/ProSP-C) in AECII and A549 cell lines. Our results showed a significant decrease in ProSP-C CD31 CD45 and CD74 CD31 CD45 expression in AECII and A549 cell line with the virus strain A(H1N1)pdm09 versus A/Victoria/3/75 (H3N2) and controls (non-infection conditions). Our findings indicate that changes in the expression of ProSP-C in AECII and A549 cell lines in infection conditions could result in dysfunction leading to decreased lung compliance, increased work of breathing and increased susceptibility to injury.

摘要

甲型流感病毒(IAV)的主要复制部位是 II 型肺泡上皮细胞(AECII),这是正常肺功能的核心,具有重要的免疫功能。表面活性剂成分主要由 AECII 合成,在宿主抵抗感染方面发挥着至关重要的作用。本研究旨在分析流感感染对 A(H1N1)pdm09 和 A/Victoria/3/75(H3N2)在感染 BALB/c 小鼠的 AECII 和感染两种病毒株的 A549 细胞系中的共刺激分子和 ProSP-C 表达的影响是否存在差异。使用大流行 A(H1N1)pdm09 和 A/Victoria/3/75(H3N2)感染 BALB/c 小鼠和 A549 细胞系。我们评估了 AECII 和 A549 细胞系中共刺激分子(CD45/CD31/CD74/ProSP-C)的表面表达。结果表明,与 A/Victoria/3/75(H3N2)和对照(非感染条件)相比,A(H1N1)pdm09 病毒株感染导致 AECII 和 A549 细胞系中 ProSP-C CD31 CD45 和 CD74 CD31 CD45 的表达显著降低。我们的发现表明,感染条件下 AECII 和 A549 细胞系中 ProSP-C 表达的变化可能导致功能障碍,从而导致肺顺应性降低、呼吸功增加和易受伤。

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