Othumpangat Sreekumar, Noti John D, McMillen Cynthia M, Beezhold Donald H
Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV, USA.
Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV, USA.
Virology. 2016 Jan;487:85-94. doi: 10.1016/j.virol.2015.10.005. Epub 2015 Oct 23.
Intercellular cell adhesion molecule-1 (ICAM-1) is an inducible cell surface glycoprotein that is expressed on many cell types. Influenza virus infection enhanced ICAM-1 expression and messenger RNA levels. Human bronchial epithelial cells (HBEpC) and nasal epithelial cells, on exposure to different strains of influenza virus (H1N1, H3N2, and H9N1) showed significant increase in ICAM-1 gene expression (p<0.001) along with the ICAM-1 protein levels (surface and secreted). Depleting ICAM-1 in HBEpC with ICAM-1 siRNA and subsequently infecting with H1N1 showed increased viral copy numbers. Influenza virus infection in HBEpC resulted in up-regulation of NF-ĸB protein and the lack of ICAM-1 decreased NF-ĸB activity in NF-ĸB luciferase reporter assay. Addition of exogenous IL-1β to HBEpC induced the ICAM-1 expression and decreased matrix gene copy number. Taken together, HBEpC induced ICAM-1 plays a key role in modulating the influenza virus survival possibly through the NF-ĸB pathway.
细胞间黏附分子-1（ICAM-1）是一种可诱导的细胞表面糖蛋白，在多种细胞类型上表达。流感病毒感染可增强ICAM-1的表达和信使RNA水平。人支气管上皮细胞（HBEpC）和鼻上皮细胞在暴露于不同株的流感病毒（H1N1、H3N2和H9N1）后，ICAM-1基因表达（p<0.001）以及ICAM-1蛋白水平（表面和分泌型）均显著增加。用ICAM-1小干扰RNA（siRNA）耗尽HBEpC中的ICAM-1，随后感染H1N1，结果显示病毒拷贝数增加。HBEpC中的流感病毒感染导致核因子-κB（NF-κB）蛋白上调，而在NF-κB荧光素酶报告基因检测中，ICAM-1的缺失降低了NF-κB活性。向HBEpC中添加外源性白细胞介素-1β（IL-1β）可诱导ICAM-1表达并降低基质基因拷贝数。综上所述，HBEpC诱导的ICAM-1可能通过NF-κB途径在调节流感病毒存活中起关键作用。
