Additional file 1: of Influenza A virus infection dysregulates the expression of microRNA-22 and its targets; CD147 and HDAC4, in epithelium of asthmatics

Figure S1. Monolayer cultures and generation of ALI-pBEC cultures from non-asthmatics and asthmatics. Figure S2. Viability of HBEC6-KT cell after IAV H1N1 infection at different MOIs. Figure S3. Responses of pBECs from non-asthmatics and asthmatics cultured as monolayers to IAV H1N1 infection. Figure S4. Responses of pBECs from non-asthmatics and asthmatics cultured at ALI to IAV H1N1 infection. Figure S5. RNU44 expression miRNA endogenous control in in pBECs from non-asthmatics and asthmatics cultured as monolayers and at ALI. Figure S6. UV-inactivated IAV H1N1 effects on levels of miRNA expression in pBECs from non-asthmatics and asthmatics. Figure S7. miR-22 mimic suppresses and antagomir increases CD147 and HDAC4 mRNA expression. (ZIP 499 kb)

补充图S1：非哮喘者与哮喘者来源的单层培养体系及气液界面原代支气管上皮细胞（ALI-pBEC）培养物的构建。
补充图S2：不同感染复数（MOI, Multiplicity of Infection）下甲型流感病毒（IAV, Influenza A Virus）H1N1感染HBEC6-KT细胞后的细胞活力。
补充图S3：单层培养的非哮喘者与哮喘者来源的原代支气管上皮细胞（pBEC, primary bronchial epithelial cells）对甲型流感病毒（IAV）H1N1感染的应答反应。
补充图S4：气液界面（ALI, Air-Liquid Interface）培养的非哮喘者与哮喘者来源的原代支气管上皮细胞（pBEC）对甲型流感病毒（IAV）H1N1感染的应答反应。
补充图S5：非哮喘者与哮喘者来源的单层及气液界面培养的原代支气管上皮细胞（pBEC）中，作为microRNA（miRNA）内参的RNU44的表达情况。
补充图S6：紫外线灭活的甲型流感病毒（IAV）H1N1对非哮喘者与哮喘者来源的原代支气管上皮细胞（pBEC）中microRNA（miRNA）表达水平的影响。
补充图S7：miR-22模拟物（mimic）可抑制CD147与HDAC4的mRNA表达，antagomir可上调二者的mRNA表达。（压缩包，499千字节）