Mechanisms of allergy and clinical immunologyIn vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects
Section snippets
Study subjects
Six subjects with allergic asthma and 5 healthy nonallergic subjects were studied (Table I). Allergic status was based on the presence of a positive skin prick test response (wheal 3 mm greater than the negative control with erythema) to common allergens.20 Asthmatic subjects had a diagnosis of asthma and bronchial hyperresponsiveness (PC20 methacholine, <8 mg/mL),20 were allergic to at least 1 allergen, and had mild-to-moderate disease, as defined by the National Institutes of Health
Epithelial cell cultures
After 2 to 3 weeks of growth at an air-liquid interface, all HNE (n = 70) and HBE (n = 84) cell cultures appeared fully confluent under the inverted microscope and showed properties resembling those of native epithelium, including an apical mucus layer and ciliated pseudostratified epithelium (Fig 1), as well as a permeability barrier, as demonstrated by a “dry” apical surface and the development of Rte, which is indicative of tight junction formation.22 Cultures also showed vectorial transport
Discussion
The 2 major findings of this study are that bronchial epithelial cells are more susceptible to infection with HRV-16 than nasal epithelial cells from the same subjects and that cultures of either airway site from asthmatic subjects did not have a higher response to HRV infection than cultures from healthy subjects. The first finding rejects our hypothesis that the predominance of upper airway symptoms with most rhinovirus infections is due to a greater susceptibility of nasal versus bronchial
References (37)
- et al.
Frequency, severity, and duration of rhinovirus infections in asthmatic and non-asthmatic individuals: a longitudinal cohort study
Lancet
(2002) - et al.
Mucociliary differentiation according to time in human nasal epithelial cell culture
Differentiation
(2002) - et al.
Respiratory viruses and exacerbations of asthma in adults
BMJ
(1993) - et al.
Effect of respiratory virus infections including rhinovirus on clinical status in cystic fibrosis
Arch Dis Child
(1995) - et al.
Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease
Eur Respir J
(2000) - et al.
Community study of role of viral infections in exacerbations of asthma in 9-11 year old children
BMJ
(1995) - et al.
Detection of rhinovirus infection of the nasal mucosa by oligonucleotide in situ hybridization
Am J Respir Cell Mol Biol
(1994) - et al.
Localization of human rhinovirus replication in the upper respiratory tract by in situ hybridization
J Infect Dis
(1995) - et al.
Quantitative and qualitative analysis of rhinovirus infection in bronchial tissues
Am J Respir Crit Care Med
(2005) - et al.
Detection of rhinovirus RNA in lower airway cells during experimentally induced infection
Am J Respir Crit Care Med
(1997)
Rhinoviruses infect the lower airways
J Infect Dis
Rhinovirus replication causes RANTES production in primary bronchial epithelial cells
Am J Respir Cell Mol Biol
Rhinovirus infection of primary cultures of human tracheal epithelium: role of ICAM-1 and IL-1beta
Am J Physiol Lung Cell Mol Physiol
Rhinovirus induces airway epithelial gene expression through double-stranded RNA and IFN-dependent pathways
Am J Respir Cell Mol Biol
Studies on the role of interleukin-12 in acute murine toxoplasmosis
Immunology
Sites of rhinovirus recovery after point inoculation of the upper airway
JAMA
Respiratory virus infection of monolayer cultures of human nasal epithelial cells
Am Rev Respir Dis
Similar frequency of rhinovirus-infectible cells in upper and lower airway epithelium
J Infect Dis
Cited by (171)
Air-Liquid interface cultures to model drug delivery through the mucociliary epithelial barrier
2023, Advanced Drug Delivery ReviewsRhinovirus infection of the airway epithelium enhances mast cell immune responses via epithelial-derived interferons
2023, Journal of Allergy and Clinical ImmunologySingle-cell transcriptomic analysis reveals key immune cell phenotypes in the lungs of patients with asthma exacerbation
2021, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Moreover, evaluating the specific function of a given molecule or a set of genes/proteins is another facet for determining the viability of a possible model framework of intracellular events, as the cost and controllability in a laboratory setting need to be considered. Furthermore, airway epithelial cells, airway smooth muscle cells, and fibroblasts can regulate subsequent immune response by the production of proinflammatory factors following exposure to the infection of respiratory viruses.62-64 For example, human airway smooth muscle cells are potent producers of IL-6 family cytokines after infection with RSV or parainfluenza virus.65
Glucocorticoids impair type I IFN signalling and enhance rhinovirus replication
2021, European Journal of PharmacologyCitation Excerpt :In this study, we investigated the effects of FP, an ICS commonly used for the management of asthma (Papi et al., 2018) and COPD (Rabe and Watz, 2017), and two novel selective non-steroidal (GRT7) and steroidal (GRT10) glucocorticoid receptor (GR) ligands in bronchial epithelial cells experimentally infected with RV. We used a wide range of concentrations (0.004–1000 nM) because we considered the clinical use of inhaler devices to deliver drugs into the airways might result in high concentrations of drug deposited locally on the upper respiratory tract, where viral infection and replication is most likely to initiate (Lopez-Souza et al., 2009; Tan et al., 2018). Compound GRT10 significantly suppressed production of the pro-inflammatory cytokines IL-6 and IL-8, similarly to FP and GRT7 but with slightly reduced potency and efficacy, typical of a partial agonist.
Pathogen Recognition Receptors and the Lung
2021, Encyclopedia of Respiratory Medicine, Second EditionRhinovirus Infection in Children—a Narrative Review
2020, Clinical Microbiology Newsletter
Supported by National Institutes of Health grant P01AI050496. S. Favoreto and P. C. Avila are currently supported by the Ernest S. Bazley Grant to Northwestern University.
Disclosure of potential conflict of interest: W. E. Finkbeiner has received research support from the Cystic Fibrosis Foundation and the National Institutes of Health. G. M. Dolganov has provided legal consultation or expert witness testimony on the topic of gene expression assays. J. H. Widdicombe has received research support from Cystic Fibrosis Research, Inc. H. A. Boushey has received research support from GlaxoSmithKline and honoraria from Genentech and Novartis and has served as a member and chair of the Health Effect's Institute's review committee. P. C. Avila has received research support from Genentech. The rest of the authors have declared that they have no conflict of interest.
- ∗
H. A. Boushey and P. C. Avila contributed equally to this work.