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Citations to this article

Mechanism of rhinovirus-induced changes in airway smooth muscle responsiveness.
H Hakonarson, … , D Campbell, M M Grunstein
H Hakonarson, … , D Campbell, M M Grunstein
Published November 1, 1998
Citation Information: J Clin Invest. 1998;102(9):1732-1741. https://doi.org/10.1172/JCI4141.
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Mechanism of rhinovirus-induced changes in airway smooth muscle responsiveness.

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Abstract

An important interplay exists between specific viral respiratory infections and altered airway responsiveness in the development and exacerbations of asthma. However, the mechanistic basis of this interplay remains to be identified. This study addressed the hypothesis that rhinovirus (RV), the most common viral respiratory pathogen associated with acute asthma attacks, directly affects airway smooth muscle (ASM) to produce proasthmatic changes in receptor-coupled ASM responsiveness. Isolated rabbit and human ASM tissue and cultured ASM cells were inoculated with human RV (serotype 16) or adenovirus, each for 6 or 24 h. In contrast to adenovirus, which had no effect, inoculation of ASM tissue with RV induced heightened ASM tissue constrictor responsiveness to acetylcholine and attenuated the dose-dependent relaxation of ASM to beta-adrenoceptor stimulation with isoproterenol. These RV-induced changes in ASM responsiveness were largely prevented by pretreating the tissues with pertussis toxin or with a monoclonal blocking antibody to intercellular adhesion molecule-1 (ICAM-1), the principal endogenous receptor for most RVs. In extended studies, we found that the RV-induced changes in ASM responsiveness were associated with diminished cAMP accumulation in response to dose-dependent administration of isoproterenol, and this effect was accompanied by autologously upregulated expression of the Gi protein subtype, Gialpha3, in the ASM. Finally, in separate experiments, we found that the RV-induced effects on ASM responsiveness were also accompanied by autologously induced upregulated mRNA and cell surface protein expression of ICAM-1. Taken together, these findings provide new evidence that RV directly induces proasthmatic phenotypic changes in ASM responsiveness, that this effect is triggered by binding of RV to its ICAM-1 receptor in ASM, and that this binding is associated with the induced endogenously upregulated expression of ICAM-1 and enhanced expression and activation of Gi protein in the RV-infected ASM.

Authors

H Hakonarson, N Maskeri, C Carter, R L Hodinka, D Campbell, M M Grunstein

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Total citations by year

Year: 2023 2020 2018 2017 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 Total
Citations: 1 1 1 2 5 5 1 5 1 1 5 9 2 6 3 2 10 3 7 4 1 75
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2012 (5)

Title and authors Publication Year
G Protein βγ-Subunit Signaling Mediates Airway Hyperresponsiveness and Inflammation in Allergic Asthma
G Nino, A Hu, JS Grunstein, J McDonough, PA Kreiger, MB Josephson, JK Choi, MM Grunstein
PloS one 2012
β2-Agonists inhibit TNF-α-induced ICAM-1 expression in human airway parasympathetic neurons
Z Nie, AD Fryer, DB Jacoby
PloS one 2012
Emerging mediators of airway smooth muscle dysfunction in asthma
B Yeganeh, C Xia, H Movassagh, C Koziol-White, Y Chang, L Al-Alwan, JE Bourke, BG Oliver
Pulmonary Pharmacology & Therapeutics 2012
Don't Forget Bordetella
FG Versteegh
American journal of respiratory and critical care medicine 2012
Virus Infection-Induced Bronchial Asthma Exacerbation
M Yamaya
Pulmonary Medicine 2012

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