NDLI: In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lopez-Souza, Nilceia Favoreto, Silvio Wong, Hofer Ward, Theresa Yagi, Shigeo Schnurr, David Finkbeiner, Walter E. Dolganov, Gregory M. Widdicombe, Jonathan H. Boushey, Homer A. Avila, Pedro C.
Description	Country affiliation: United States Author Affiliation: Lopez-Souza N ( Department of Medicine, University of California, San Francisco, Calif., USA.)
Abstract	BACKGROUND: Human rhinoviruses (HRVs) characteristically cause upper respiratory tract infection, but they also infect the lower airways, causing acute bronchitis and exacerbating asthma. OBJECTIVE: Our purpose was to study ex vivo the differences in the response to HRV infection of nasal and bronchial epithelial cultures from the same healthy and asthmatic individuals using conditions favoring development of fully differentiated, pseudostratified mucociliary epithelium. METHODS: Cells from the inferior turbinates and bronchial tree of 5 healthy and 6 asthmatic individuals were cultured at an air-liquid interface. Cultures were infected with HRV-16, and after 48 hours, the degree of infection was measured. RESULTS: Baseline median transepithelial resistance was lower in human bronchial epithelial (HBE) cell cultures than in human nasal epithelial (HNE) cell cultures (195 Omega.cm2 [95% CI, 164-252] vs 366 Omega.cm2 [95% CI, 234-408], respectively; P < .01). Virus replicated more easily in HBE cells than in HNE cells based on virus shedding in apical wash (log tissue culture infective dose of 50%/0.1 mL = 2.0 [95% CI, 1.0-2.5] vs 0.5 [95% CI, 0.5-1.5], P < .01) and on a 20- to 30-fold greater viral load and number of infected cells in HBE cell cultures than in HNE cell cultures. The increases in expression of RANTES and double-stranded RNA-dependent protein kinase were greater in HBE cell cultures than in HNE cell cultures, as were the concentrations of IL-8, IL-1alpha, RANTES, and IP-10 in basolateral medium. However, no significant differences between asthmatic and healthy subjects (including IFN-beta1 expression) were found. CONCLUSIONS: Differentiated nasal epithelial cells might have mechanisms of increased resistance to rhinovirus infection compared with bronchial epithelial cells. We could not confirm previous reports of increased susceptibility to HRV infection in epithelial cells from asthmatic subjects.
File Format	HTM / HTML
ISSN	00916749
e-ISSN	10976825
DOI	10.1016/j.jaci.2009.03.010
Journal	Journal of Allergy and Clinical Immunology
Issue Number	6
Volume Number	123
Language	English
Publisher	Elsevier
Publisher Date	2009-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Immunology Asthma Virology Bronchi Nasal Cavity Picornaviridae Infections Immunology Respiratory Mucosa Rhinovirus Cells, Cultured Cytokines Metabolism Intercellular Adhesion Molecule-1 Virus Replication Comparative Study Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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