ArticleThe Journal of clinical investigation1998
Mechanism of rhinovirus-induced changes in airway smooth muscle responsiveness.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 78 citations in OpenAlex.
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- The use of βERJ open research · 2020Review
- Modulation of airway hyperresponsiveness by rhinovirus exposure.Respiratory research · 2018Review
- Coupling of Airway Smooth Muscle Bitter Taste Receptors to Intracellular Signaling and Relaxation Is via GAmerican journal of respiratory cell and molecular biology · 2017Article
- TLR3 activation increases chemokine expression in human fetal airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Glucocorticoid genes and the developmental origins of asthma susceptibility and treatment response.American journal of respiratory cell and molecular biology · 2015Article
- Infection in severe asthma exacerbations and critical asthma syndrome.Clinical reviews in allergy & immunology · 2015Review
- The importance of bacterial and viral infections associated with adult asthma exacerbations in clinical practice.PloS one · 2015Article
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- Article
- G Protein βγ-subunit signaling mediates airway hyperresponsiveness and inflammation in allergic asthma.PloS one · 2012Article
- Virus infection-induced bronchial asthma exacerbation.Pulmonary medicine · 2012Article
- β2-Agonists inhibit TNF-α-induced ICAM-1 expression in human airway parasympathetic neurons.PloS one · 2012Article
- Primary murine airway smooth muscle cells exposed to poly(I,C) or tunicamycin synthesize a leukocyte-adhesive hyaluronan matrix.The Journal of biological chemistry · 2009Article
- Activation of endogenous GABAA channels on airway smooth muscle potentiates isoproterenol-mediated relaxation.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- Human rhinoviruses: the cold wars resume.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2008Review
- Regulation of heterotrimeric G protein signaling in airway smooth muscle.Proceedings of the American Thoracic Society · 2008Review
- Crosstalk between Gi and Gq/Gs pathways in airway smooth muscle regulates bronchial contractility and relaxation.The Journal of clinical investigation · 2007Article
- Mechanisms of virus-induced asthma exacerbations: state-of-the-art. A GA2LEN and InterAirways document.Allergy · 2007Review
- Increased proinflammatory responses from asthmatic human airway smooth muscle cells in response to rhinovirus infection.Respiratory research · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.