A role for airway remodeling during respiratory syncytial virus infection

Becnel, David; You, Dahui; Erskin, J.; Dimina, Dawn; Cormier, Stephania A.

doi:10.1186/1465-9921-6-122

Cited by 44 publications

(50 citation statements)

References 44 publications

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“…Baseline R values in normal BALB/c mice were similar to those reported previously (3). Baseline changes in lung function comparable with those we (5) reported previously were found in the current study (data not shown): a significant increase in baseline airway resistance (R) at 2 d.p.i., but not at other time points after infection, as well as nonsignificant increases in Newtonian (central airway) resistance (R N ), tissue damping (G), and tissue elastance (H) at this time point.…”

Section: Effect Of Rsv Infection On Basal Lung Mechanics and Responsisupporting

confidence: 92%

“…Unlike whole body plethysmography, however, it is invasive and so does not permit serial measurements from the same animal. Only a limited number of studies to date have employed the flexiVent to determine the effects of RSV on airway function in mice (3,27,42), and no previous studies have evaluated ␤-agonist responses in RSV-infected animals using this system.…”

Section: Discussionmentioning

confidence: 99%

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Respiratory syncytial virus induces airway insensitivity to β-agonists in BALB/c mice

Traylor

Davis

2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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Adrenergic agonists (␤-agonists) are commonly used to treat respiratory syncytial virus (RSV) bronchiolitis but are generally ineffective for unknown reasons. We have previously shown that RSV strain A2 inhibits bronchoalveolar epithelial responses to ␤-agonists in a BALB/c mouse model by inducing heterologous keratinocyte cytokine (KC)/CXCR2-mediated desensitization of epithelial ␤ 2-adrenergic receptors. The aim of the current study was to determine whether RSV also induces airway insensitivity to ␤-agonists. Total lung resistance (R) was measured in anesthetized female BALB/c mice undergoing mechanical ventilation on a flexiVent computer-controlled piston ventilator. Data were analyzed using the single-compartment model. Infection with RSV A2 did not induce airway hyperresponsiveness to increasing doses of the nebulized cholinergic agonist methacholine (MCh) at any time point after RSV infection. Prenebulization with the ␤-agonist terbutaline (100 M) significantly attenuated bronchoconstrictive responses to 20 and 50 mg/ml MCh in uninfected mice and in mice infected with RSV 4 -8 days postinfection (d.p.i.). However, in mice infected with replication-competent, but not UV-inactivated, RSV for 2 days, significant terbutaline insensitivity was found. Terbutaline insensitivity at 2 d.p.i. could be reversed by systemic preinfection treatment with neutralizing anti-CXCR2 antibodies, which reduced bronchoalveolar lavage (BAL) neutrophil counts but did not alter viral replication, BAL KC levels, or lung edema. Terbutaline insensitivity was also reversed by postinfection nebulization with neutralizing anti-KC or anti-CXCR2 antibodies and could be replicated in normal, uninfected mice by nebulization with recombinant KC. These data suggest that KC/CXCR2-mediated airway insensitivity to ␤-agonists may underlie the modest utility of these drugs as bronchodilators in therapy for acute RSV bronchiolitis. CXCL8; CXCR2; keratinocyte cytokine; airway hyperresponsiveness RESPIRATORY SYNCYTIAL VIRUS (RSV) is the most common cause of lower respiratory tract disease in infants and children worldwide (36). In the United States, 50 -70% of infants are infected with RSV in the first year of life (29) with bronchiolitis now accounting for approximately 75,000 -125,000 hospitalizations annually (32, 33). RSV-related mortality has decreased over the last 20 yr, but RSV remains the leading cause of viral deaths in infants (33). In addition, this virus is increasingly recognized as being underdiagnosed as a cause of communityacquired lower respiratory tract infections among adults (10) and is a significant cause of excess morbidity and mortality in immune-compromised adults (41). Indeed, recent studies suggest that RSV has a disease impact comparable with that of nonpandemic influenza A in the elderly (9).

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Section: Effect Of Rsv Infection On Basal Lung Mechanics and Responsisupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus induces airway insensitivity to β-agonists in BALB/c mice

Traylor

Davis

2010

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…5A) and were similar to those reported previously (1). Likewise, exposure to nebulized terbutaline had no effect on baseline total lung resistance values in either saline-or poly(I:C)-treated mice (Fig.…”

Section: Intranasal Exposure To the Double-stranded Rna Analog Poly(isupporting

confidence: 90%

“…For assessment of ␤-agonist responsiveness, a second, age-matched, group of female mice was evaluated in parallel for each treatment condition. As in previous studies (55), initial baseline measurements of lung function with nebulization of saline were followed by exposure to the nebulized ␤-agonist terbutaline (100 M), then increasing doses of methacholine (1,10,20, and 50 mg/ml), with a further dose of ␤-agonist between each dose of methacholine. Average values of 10 total lung-resistance measurements at each methacholine or terbutaline dose were thereby obtained, and percent changes from baseline were calculated, as above.…”

Section: Methodsmentioning

confidence: 99%

Double-stranded RNA induces similar pulmonary dysfunction to respiratory syncytial virus in BALB/c mice

Aeffner

Traylor

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…TNF-a is known as a potent mediator of inflammation and plays a key role during the inflammatory responses of hRSV bronchiolitis (Becnel et al, 2005;McNamara et al, 2004;Morrison et al, 2007). TNF-a may play a protective role in RSV infection (Neuzil et al, 1996).…”

Section: A F G Antonis and Othersmentioning

confidence: 99%

Age-dependent differences in the pathogenesis of bovine respiratory syncytial virus infections related to the development of natural immunocompetence

Antonis

Jong

Poel

et al. 2010

Journal of General Virology

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A role for airway remodeling during respiratory syncytial virus infection

Cited by 44 publications

References 44 publications

Respiratory syncytial virus induces airway insensitivity to β-agonists in BALB/c mice

Respiratory syncytial virus induces airway insensitivity to β-agonists in BALB/c mice

Double-stranded RNA induces similar pulmonary dysfunction to respiratory syncytial virus in BALB/c mice

Age-dependent differences in the pathogenesis of bovine respiratory syncytial virus infections related to the development of natural immunocompetence

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