呼吸道合胞病毒免疫和感染后，对小鼠肺部疾病有影响的先天性和适应性细胞表型。

Innate and adaptive cellular phenotypes contributing to pulmonary disease in mice after respiratory syncytial virus immunization and infection.

作者信息

Lee Young-Tae, Kim Ki-Hye, Hwang Hye Suk, Lee Youri, Kwon Young-Man, Ko Eun-Ju, Jung Yu-Jin, Lee Yu-Na, Kim Min-Chul, Kang Sang-Moo

机构信息

Center for Inflammation, Immunity & Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA.

Center for Inflammation, Immunity & Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA; Department of Biology, Georgia State University, Atlanta, GA 30303, USA.

出版信息

Virology. 2015 Nov;485:36-46. doi: 10.1016/j.virol.2015.07.001. Epub 2015 Jul 18.

Respiratory syncytial virus (RSV) is the major leading cause of infantile viral bronchiolitis. However, cellular phenotypes contributing to the RSV protection and vaccine-enhanced disease remain largely unknown. Upon RSV challenge, we analyzed phenotypes and cellularity in the lung of mice that were naïve, immunized with formalin inactivated RSV (FI-RSV), or re-infected with RSV. In comparison with naïve and live RSV re-infected mice, the high levels of eosinophils, neutrophils, plasmacytoid and CD11b(+) dendritic cells, and IL-4(+) CD4(+) T cells were found to be contributing to pulmonary inflammation in FI-RSV immune mice despite lung viral clearance. Alveolar macrophages appeared to play differential roles in protection and inflammation upon RSV infection of different RSV immune mice. These results suggest that multiple innate and adaptive immune components differentially contribute to RSV disease and inflammation.

呼吸道合胞病毒（RSV）是婴儿病毒性细支气管炎的主要病因。然而，有助于RSV保护和疫苗增强疾病的细胞表型在很大程度上仍不清楚。在RSV攻击后，我们分析了未接触过病毒、用福尔马林灭活RSV（FI-RSV）免疫或再次感染RSV的小鼠肺中的表型和细胞组成。与未接触过病毒和再次感染活RSV的小鼠相比，尽管肺内病毒已清除，但在FI-RSV免疫小鼠中发现高水平的嗜酸性粒细胞、中性粒细胞、浆细胞样细胞和CD11b(+)树突状细胞以及IL-4(+) CD4(+) T细胞会导致肺部炎症。在不同RSV免疫小鼠感染RSV后，肺泡巨噬细胞在保护和炎症反应中似乎发挥着不同作用。这些结果表明，多种先天性和适应性免疫成分对RSV疾病和炎症有不同的影响。