Airway function and reactivity, leukocyte influx and nitric oxide after inoculation with parainfluenza-3 virus: effects of dexamethasone or rolipram

Toward, Toby J.; Johnson, Frederick J.; Boult, J. E.; Maillard, Jean‐Yves

doi:10.1016/j.intimp.2004.12.006

Cited by 9 publications

(10 citation statements)

References 38 publications

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“…Inoculation of guinea pigs with parainfluenza-3 virus caused AHR to inhaled histamine and inflammatory cell influx into the BALF, in agreement with previous studies (Folkerts et al, 2000;Toward et al, 2005). The B 2 receptor antagonist MEN16132 and the tissue kallikrein inhibitor VA999024 (Evans et al, 1996) abolished these effects after PIV-3 inoculation.…”

Section: Discussionsupporting

confidence: 90%

“…In this study, we therefore determined whether ovalbumin exposure in ovalbumin-sensitized guinea pigs produced AHR to inhaled bradykinin. AHR is also a consequence of viral infection of the airways and has been shown along with an influx of inflammatory cells after inoculation of guinea pigs with parainfluenze-3 virus (PIV-3) (Toward et al, 2005). Folkerts et al (2000) showed that the bradykinin B 2 antagonist icatibant can inhibit AHR induced by PIV-3 but not the inflammatory cell influx.…”

Section: Introductionmentioning

confidence: 99%

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Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Broadley

Blair²,

Kidd³

et al. 2010

J Pharmacol Exp Ther

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Inhaled bradykinin causes bronchoconstriction in asthmatic subjects but not nonasthmatics. To date, animal studies with inhaled bradykinin have been performed only in anesthetized guinea pigs and rats, where it causes bronchoconstriction through sensory nerve pathways. In the present study, airway function was recorded in conscious guinea pigs by whole-body plethysmography. Inhaled bradykinin (1 mM, 20 s) caused bronchoconstriction and influx of inflammatory cells to the lungs, but only when the enzymatic breakdown of bradykinin by angiotensin-converting enzyme and neutral endopeptidase was inhibited by captopril (1 mg/kg i.p.) and phosphoramidon (10 mM, 20-min inhalation), respectively. The bronchoconstriction and cell influx were antagonized by the B 2 kinin receptor antagonist 4-(S)-amino-5-(4-{4-[2, 4-dichloro-3-(2,4-dimethyl-8-quinolyloxymethyl)phenylsulfonamido]-tetrahydro-2H-4-pyranylcarbonyl}piperazino)-5-oxopentyl](trimethyl)ammonium chloride hydrochloride (MEN16132) when given by inhalation (1 and 10 M, 20 min) and are therefore mediated via B 2 kinin receptors. However, neither intraperitioneal MEN16132 nor the peptide B 2 antagonist icatibant, by inhalation, antagonized these bradykinin responses. Sensitization of guinea pigs with ovalbumin was not sufficient to induce airway hyperreactivity (AHR) to the bronchoconstriction by inhaled bradykinin. However, ovalbumin challenge of sensitized guinea pigs caused AHR to bradykinin and histamine. Infection of guinea pigs by nasal instillation of parainfluenza-3 virus produced AHR to inhaled histamine and lung influx of inflammatory cells. These responses were attenuated by the bradykinin B 2 receptor antagonist MEN16132 and H-(4-chloro)DPhe-2Ј(1-naphthylalanine)-(3-aminopropyl)guanidine (VA999024), an inhibitor of tissue kallikrein, the enzyme responsible for lung synthesis of bradykinin. These results suggest that bradykinin is involved in virus-induced inflammatory cell influx and AHR.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Broadley

Blair²,

Kidd³

et al. 2010

J Pharmacol Exp Ther

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“…As a chronic inflammatory disease, COPD responds poorly to currently available therapies, particularly corticosteroids [11,12], suggesting that the inflammation in COPD is essentially corticosteroid resistant. An important mechanism of increased inflammatory response in COPD, which is also linked to corticosteroid resistance, is a reduction in the critical nuclear enzyme histone deacetylase (HDAC)2 [13].…”

Section: Introductionmentioning

confidence: 99%

Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity

Bao

et al. 2012

International Immunopharmacology

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“…hPIV-3 (human parainfluenza type-3 virus) causes pulmonary inflammation and airways hyper-responsiveness in guinea-pigs as we [26,27] and others [20,28,29] have previously reported. One study in particular reported that pulmonary inflammation induced by bovine parainfluenza type-3 virus was sensitive to beclamethasone treatment but the airway hyper-responsiveness was insensitive [30].…”

Section: Introductionmentioning

confidence: 76%

“…One of the aims of our study was to examine whether viral exacerbation of allergy-induced pulmonary inflammation generated a glucocorticoid-resistant phenotype. For this reason, together with our previous experience [26,27], we elected to use hPIV-3 in the present study.…”

Section: Introductionmentioning

confidence: 99%

Human parainfluenza type 3 virus impairs the efficacy of glucocorticoids to limit allergy-induced pulmonary inflammation in guinea-pigs

et al. 2013

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Viral exacerbations of allergen-induced pulmonary inflammation in pre-clinical models reportedly reduce the efficacy of glucocorticoids to limit pulmonary inflammation and airways hyper-responsiveness to inhaled spasmogens. However, exacerbations of airway obstruction induced by allergen challenge have not yet been studied. hPIV-3 (human parainfluenza type 3 virus) inoculation of guinea-pigs increased inflammatory cell counts in BAL (bronchoalveolar lavage) fluid and caused hyper-responsiveness to inhaled histamine. Both responses were abolished by treatment with either dexamethasone (20 mg/kg of body weight, subcutaneous, once a day) or fluticasone propionate (a 0.5 mg/ml solution aerosolized and inhaled over 15 min, twice a day). In ovalbumin-sensitized guinea-pigs, allergen (ovalbumin) challenge caused two phases of airway obstruction [measured as changes in sGaw (specific airways conductance) using whole body plethysmography]: an immediate phase lasting between 4 and 6 h and a late phase at about 7 h. The late phase, airway hyper-responsiveness to histamine and inflammatory cell counts in BAL were all significantly reduced by either glucocorticoid. Inoculation of guinea-pigs sensitized to ovalbumin with hPIV-3 transformed the allergen-induced airway obstruction from two transient phases into a single sustained response lasting up to 12 h. This exacerbated airway obstruction and airway hyper-responsiveness to histamine were unaffected by treatment with either glucocorticoid whereas inflammatory cell counts in BAL were only partially inhibited. Virus- or allergen-induced pulmonary inflammation, individually, are glucocorticoid-sensitive, but in combination generate a phenotype where glucocorticoid efficacy is impaired. This suggests that during respiratory virus infection, glucocorticoids might be less effective in limiting pulmonary inflammation associated with asthma.

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Airway function and reactivity, leukocyte influx and nitric oxide after inoculation with parainfluenza-3 virus: effects of dexamethasone or rolipram

Cited by 9 publications

References 38 publications

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Bradykinin-Induced Lung Inflammation and Bronchoconstriction: Role in Parainfluenze-3 Virus-Induced Inflammation and Airway Hyperreactivity

Baicalin is anti-inflammatory in cigarette smoke-induced inflammatory models in vivo and in vitro: A possible role for HDAC2 activity

Human parainfluenza type 3 virus impairs the efficacy of glucocorticoids to limit allergy-induced pulmonary inflammation in guinea-pigs

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