Rhinovirus Induction of the CXC Chemokine Epithelial-Neutrophil Activating Peptide-78 in Bronchial Epithelium

• Published in: The Journal of infectious diseases Vol. 187; no. 11; pp. 1809 - 1817
• Main Authors: Donninger, Howard, Glashoff, Richard, Haitchi, Hans-Michael, Syce, James A., Ghildyal, Reena, van Rensburg, Estrelita, Bardin, Philip G.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 01.06.2003; University of Chicago Press; Oxford University Press
• Subjects: Adult; Asthma; Asthma - metabolism; Biological and medical sciences; Bronchi - metabolism; Cell Line; Cell lines; Cells, Cultured; Chemokine CXCL5; Chemokines; Chemokines, CXC - biosynthesis; Chemokines, CXC - genetics; Chemokines, CXC - metabolism; Epithelial cells; Epithelium - metabolism; Female; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation; HeLa cells; Humans; Infections; Interleukin-8 - analogs & derivatives; Interleukin-8 - biosynthesis; Interleukin-8 - genetics; Interleukin-8 - metabolism; Male; Messenger RNA; Microbiology; Neutrophils; Picornaviridae Infections - genetics; Picornaviridae Infections - metabolism; Promoter Regions, Genetic; Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains; Rhinovirus; Rhinovirus - physiology; RNA, Messenger - genetics; RNA, Messenger - metabolism; Time Factors; Transcription, Genetic; Virology; Virus Replication; Viruses; Virus; Respiratory tract; Picornaviridae; Pathogenesis; Bronchus; Inflammation; Neutrophil; CXC chemokine; Epithelium; Respiratory system; Host virus relation; Rhinovirus
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/375246

Epithelial-neutrophil activating peptide-78 (ENA-78) induces neutrophil migration, an early response to viral infection. Rhinovirus serotype 16 (RV16) was used to infect primary bronchial epithelial cells and a cell line (BEAS-2B). Release of ENA-78 protein was measured by enzyme-linked immunosorbent assay, ENA-78 mRNA production was quantified by reverse-transcription polymerase chain reaction, and ENA-78 promoter activity was assessed by use of a promoter construct. After infection with RV16, ENA-78 protein and mRNA increased significantly, and RV16 induced 3-fold increases in ENA-78 gene transcription. Nasal ENA-78 measured in patients with asthma with and without RV infection was more elevated in patients with RV infection present. Our study demonstrates that ENA-78 is produced in bronchial epithelial cells in response to RV16 infection. With other chemokines, it may be an important initiator of neutrophil airway inflammation during RV common colds and thus may play a role in the development of virus-associated airway pathologies