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Rat coronaviruses infect rat alveolar type I epithelial cells and induce expression of CXC chemokines.

机译:大鼠冠状病毒感染大鼠I型肺泡上皮细胞并诱导CXC趋化因子的表达。

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摘要

We analyzed the ability of two rat coronavirus (RCoV) strains, sialodacryoadenitis virus (SDAV) and Parker's RCoV (RCoV-P), to infect rat alveolar type I cells and induce chemokine expression. Primary rat alveolar type II cells were transdifferentiated into the type I cell phenotype. Type I cells were productively infected with SDAV and RCoV-P, and both live virus and UV-inactivated virus induced mRNA and protein expression of three CXC chemokines: CINC-2, CINC-3, and LIX, which are neutrophil chemoattractants. Dual immunolabeling of type I cells for viral antigen and CXC chemokines showed that chemokines were expressed primarily by uninfected cells. Virus-induced chemokine expression was reduced by the IL-1 receptor antagonist, suggesting that IL-1 produced by infected cells induces uninfected cells to express chemokines. Primary cultures of alveolar epithelial cells are an important model for the early events in viral infection that lead to pulmonary inflammation.
机译:我们分析了两种大鼠冠状病毒(RCoV)株,唾液酸腺腺炎病毒(SDAV)和帕克氏RCoV(RCoV-P)感染大鼠I型肺泡并诱导趋化因子表达的能力。将大鼠原发性II型肺泡细胞转分化为I型细胞表型。 I型细胞被SDAV和RCoV-P高效感染,活病毒和紫外线灭活病毒都诱导了三种CXC趋化因子CINC-2,CINC-3和LIX的mRNA和蛋白质表达,它们是中性粒细胞趋化因子。 I型细胞对病毒抗原和CXC趋化因子的双重免疫标记显示,趋化因子主要由未感染的细胞表达。 IL-1受体拮抗剂可降低病毒诱导的趋化因子表达,表明感染细胞产生的IL-1诱导未感染细胞表达趋化因子。肺泡上皮细胞的原代培养是导致肺部炎症的病毒感染早期事件的重要模型。

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