ICAM-1 regulates the survival of influenza virus in lung epithelial cells during the early stages of infection.
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.
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. Electronic address: seo8@cdc.gov.
Sreekumar
S
Othumpangat
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.
John D
JD
Noti
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.
Cynthia M
CM
McMillen
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.
Donald H
DH
Beezhold
D000818:Animals; D001980:Bronchi / Q000276:immunology / Q000821:virology; D002460:Cell Line; D004285:Dogs; D004847:Epithelial Cells / Q000821:virology; D005109:Extracellular Matrix / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D053118:Influenza A Virus, H1N1 Subtype / Q000276:immunology*; D053122:Influenza A Virus, H3N2 Subtype / Q000276:immunology*; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis / Q000235:genetics / Q000276:immunology*; D053583:Interleukin-1beta / Q000494:pharmacology; D061985:Madin Darby Canine Kidney Cells; D034622:RNA Interference; D034741:RNA, Small Interfering; D020545:Respiratory Mucosa / Q000166:cytology / Q000276:immunology* / Q000821:virology; D051996:Transcription Factor RelA / Q000096:biosynthesis / Q000378:metabolism*
C508585:IL1B protein, human; D053583:Interleukin-1beta; C498143:RELA protein, human; D034741:RNA, Small Interfering; D051996:Transcription Factor RelA; D018799:Intercellular Adhesion Molecule-1
Influenza virus; Intercellular cell adhesion molecule; Lung epithelial cells; NF-κB; Signaling