ArticleAmerican journal of respiratory cell and molecular biology2006
Respiratory syncytial virus infection reduces beta2-adrenergic responses in human airway smooth muscle.
Article in American journal of respiratory cell and molecular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- Update on the Role of β2AR and TRPV1 in Respiratory Diseases.International journal of molecular sciences · 2024Review
- An overview on the RSV-mediated mechanisms in the onset of non-allergic asthma.Frontiers in pediatrics · 2022Review
- Respiratory syncytial virus induces βScience signaling · 2021Article
- TLR3 activation increases chemokine expression in human fetal airway smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Targeting airway smooth muscle in airways diseases: an old concept with new twists.Expert review of respiratory medicine · 2011Review
- Nasal potential difference to detect Na+ channel dysfunction in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2011Review
- Post-infection A77-1726 blocks pathophysiologic sequelae of respiratory syncytial virus infection.American journal of respiratory cell and molecular biology · 2007Article
- Respiratory syncytial virus induces insensitivity to beta-adrenergic agonists in mouse lung epithelium in vivo.American journal of physiology. Lung cellular and molecular physiology · 2007Article
- Epithelial sodium channels in the adult lung--important modulators of pulmonary health and disease.Advances in experimental medicine and biology · 2007Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Although respiratory syncytial virus (RSV) is the most common cause of lower respiratory tract illness in infants, the effect of RSV on human airway smooth muscle (HASM) has not been studied. We hypothesized that RSV has direct effects on cAMP formation and beta(2)-adrenergic receptor (ADRB2) density and that ADRB2 haplotype influences this response. A recombinant green-fluorescent protein (rg) expressing RSV was used to determine whether RSV could infect cultured HASM. Influence of RSV infection on beta(2)-adrenergic responsiveness was determined by measuring differences in isoproterenol (ISO)-induced cyclic AMP (cAMP) formation, ADRB2 density, and G(i) expression in HASM cells challenged with RSV, with ultraviolet-inactivated RSV, and with mock infection. The rgRSV efficiently infected cultured HASM cells. ISO-induced cAMP formation was significantly reduced in cells infected with RSV, compared with mock-infected and ultraviolet-inactivated RSV, in a time- and concentration-dependent manner. Forskolin-induced cAMP formation and Gi expression were not altered in cells infected with RSV, suggesting that the influence of RSV on beta(2)-adrenergic relaxation was upstream of cAMP formation. ADRB2 density was reduced in cells infected with RSV, compared with mock infection, and the Arg16Gln27 ADRB2 haplotype was associated with decreased ISO-induced cAMP formation (P < 0.05) and with decreased ADRB2 density at baseline (P < 0.05). The implications of these results are that limitations of beta(2)-agonists in the treatment of any airway obstruction associated with RSV infection may be related to direct effects of RSV on HASM, and ADRB2 genotype may predict beta(2)-adrenergic responses.
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Registered trials
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