Modulation of airway hyperresponsiveness by rhinovirus exposure
Abstract Rhinovirus (RV) exposure has been implicated in childhood development of wheeze evoking asthma and exacerbations of underlying airways disease. Studies such as the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) and Childhood Origins of ASThma (COAST) have identified RV as a...
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doaj-d9950dedf53643fbb380a153f966f6342020-11-25T01:46:10ZengBMCRespiratory Research1465-993X2018-10-0119111110.1186/s12931-018-0914-9Modulation of airway hyperresponsiveness by rhinovirus exposureDennis Lo0Joshua L. Kennedy1Richard C. Kurten2Reynold A. Panettieri3Cynthia J. Koziol-White4Department of Medicine, Rutgers Institute for Translational Medicine and Science, Rutgers UniversityDepartment of Pediatrics, Division of Allergy and Immunology, University of Arkansas for Medical SciencesDepartment of Physiology and Biophysics, University of Arkansas for Medical SciencesDepartment of Medicine, Rutgers Institute for Translational Medicine and Science, Rutgers UniversityDepartment of Medicine, Rutgers Institute for Translational Medicine and Science, Rutgers UniversityAbstract Rhinovirus (RV) exposure has been implicated in childhood development of wheeze evoking asthma and exacerbations of underlying airways disease. Studies such as the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) and Childhood Origins of ASThma (COAST) have identified RV as a pathogen inducing severe respiratory disease. RVs also modulate airway hyperresponsiveness (AHR), a key characteristic of such diseases. Although potential factors underlying mechanisms by which RV induces AHR have been postulated, the precise mechanisms of AHR following RV exposure remain elusive. A challenge to RV-related research stems from inadequate models for study. While human models raise ethical concerns and are relatively difficult in terms of subject recruitment, murine models are limited by susceptibility of infection to the relatively uncommon minor group (RV-B) serotypes, strains that are generally associated with infrequent clinical respiratory virus infections. Although a transgenic mouse strain that has been developed has enhanced susceptibility for infection with the common major group (RV-A) serotypes, few studies have focused on RV in the context of allergic airways disease rather than understanding RV-induced AHR. Recently, the receptor for the virulent RV-C CDHR3, was identified, but a dearth of studies have examined RV-C-induced effects in humans. Currently, the mechanisms by which RV infections modulate airway smooth muscle (ASM) shortening or excitation-contraction coupling remain elusive. Further, only one study has investigated the effects of RV on bronchodilatory mechanisms, with only speculation as to mechanisms underlying RV-mediated modulation of bronchoconstriction.http://link.springer.com/article/10.1186/s12931-018-0914-9RhinovirusAirway HyperresponsivenessAirway smooth muscleInflammation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Dennis Lo Joshua L. Kennedy Richard C. Kurten Reynold A. Panettieri Cynthia J. Koziol-White |
spellingShingle |
Dennis Lo Joshua L. Kennedy Richard C. Kurten Reynold A. Panettieri Cynthia J. Koziol-White Modulation of airway hyperresponsiveness by rhinovirus exposure Respiratory Research Rhinovirus Airway Hyperresponsiveness Airway smooth muscle Inflammation |
author_facet |
Dennis Lo Joshua L. Kennedy Richard C. Kurten Reynold A. Panettieri Cynthia J. Koziol-White |
author_sort |
Dennis Lo |
title |
Modulation of airway hyperresponsiveness by rhinovirus exposure |
title_short |
Modulation of airway hyperresponsiveness by rhinovirus exposure |
title_full |
Modulation of airway hyperresponsiveness by rhinovirus exposure |
title_fullStr |
Modulation of airway hyperresponsiveness by rhinovirus exposure |
title_full_unstemmed |
Modulation of airway hyperresponsiveness by rhinovirus exposure |
title_sort |
modulation of airway hyperresponsiveness by rhinovirus exposure |
publisher |
BMC |
series |
Respiratory Research |
issn |
1465-993X |
publishDate |
2018-10-01 |
description |
Abstract Rhinovirus (RV) exposure has been implicated in childhood development of wheeze evoking asthma and exacerbations of underlying airways disease. Studies such as the Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) and Childhood Origins of ASThma (COAST) have identified RV as a pathogen inducing severe respiratory disease. RVs also modulate airway hyperresponsiveness (AHR), a key characteristic of such diseases. Although potential factors underlying mechanisms by which RV induces AHR have been postulated, the precise mechanisms of AHR following RV exposure remain elusive. A challenge to RV-related research stems from inadequate models for study. While human models raise ethical concerns and are relatively difficult in terms of subject recruitment, murine models are limited by susceptibility of infection to the relatively uncommon minor group (RV-B) serotypes, strains that are generally associated with infrequent clinical respiratory virus infections. Although a transgenic mouse strain that has been developed has enhanced susceptibility for infection with the common major group (RV-A) serotypes, few studies have focused on RV in the context of allergic airways disease rather than understanding RV-induced AHR. Recently, the receptor for the virulent RV-C CDHR3, was identified, but a dearth of studies have examined RV-C-induced effects in humans. Currently, the mechanisms by which RV infections modulate airway smooth muscle (ASM) shortening or excitation-contraction coupling remain elusive. Further, only one study has investigated the effects of RV on bronchodilatory mechanisms, with only speculation as to mechanisms underlying RV-mediated modulation of bronchoconstriction. |
topic |
Rhinovirus Airway Hyperresponsiveness Airway smooth muscle Inflammation |
url |
http://link.springer.com/article/10.1186/s12931-018-0914-9 |
work_keys_str_mv |
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