Optimisation of the sensitisation conditions for an ovalbumin challenge model of asthma

Smith, Nicola J.; Broadley, Kenneth J.

doi:10.1016/j.intimp.2006.09.007

Cited by 40 publications

(48 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Allergen sensitization and challenge has been repeatedly shown to cause AHR in guinea pigs to a range of spasmogens, including histamine and methacholine (Toward and Broadley, 2004;Smith and Broadley, 2007). AHR to intravenous bradykinin has been demonstrated in anesthetized rats after allergen challenge (Ellis et al, 2004), but there are few studies examining AHR to inhaled bradykinin in conscious animals.…”

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

Self Cite

View full text Add to dashboard Cite

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.

show abstract

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

Self Cite

View full text Add to dashboard Cite

show abstract

“…In sensitization of the animals, ovalbumin (OVA) was used (Smith & Broadley, 2007). Guinea pigs actively sensitized with ovalbumin provide a well-established animal model that has been used extensively for studying the pathogenic mechanisms and therapeutic treatments of bronchial hyper-responsiveness; because many of their pathophysiological features closely resemble those seen in asthmatic patients (Wu et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Eosinophils are the predominant cell type during the late asthmatic response to allergens, with their numbers peaking 24 h after allergen challenge (Smith & Broadley, 2007;Toward & Broadley, 2004). Eosinophils release many biological products including eicosanoids, oxygenfree radicals, Th2 cytokines, growth factors, and toxic granule products which contribute to contraction of smooth muscle, airways hyper responsiveness and increased vascular permeability (Bousquet et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Anti-asthmatic property and possible mode of activity of an ethanol leaf extract ofPolyscias fruticosa

Koffuor

Boye

Kyei

et al. 2015

Pharmaceutical Biology

View full text Add to dashboard Cite

Context: Polyscias fruticosa (L.) Harms (Araliaceae) is used as a traditional remedy for asthma in Ghana.Objective: The objective of this study is to establish the anti-asthmatic property and a possible mode of activity of an ethanol leaf extract of P. fruticosa (PFE). Materials and methods: The time (min) for pre-convulsive dyspnea, and time for recovery, after sensitization with 150 mg OVA and induction of bronchospasm with 1% acetylcholine or histamine in normal, and 100, 250, and 500 mg/kg PFE-treated Dunkin Hartley guinea pigs, were recorded. Atropine (0.1 mg), mepyramine (0.1 mg), and PFE (1 mg) effect on a contractile response of 2.0 Â 10 À2 mg/ml acetylcholine and 5.8 Â 10 À2 mg/ml histamine on the isolated guinea pig ileum was investigated. Cytological and histological studies were conducted using guinea pig peritoneal mast cells and mesenteric cells, respectively, to establish PFE effect on compound 48/80-induced mast cell degranulation. Results: PFE (100-500 mg/kg) prolonged the onset of pre-convulsive dyspnea by 76.1-180.2% (p 0.01-0.001), and decreased recovery time by 71.9-78.5% (p 0.01-0.001). It also enhanced percentage protection against histamine-induced bronchospasm by 15.8-80.1-fold (p 0.05-0.01), and decreased percentage recovery time 2.5-3.3-fold (p 0.05-0.01). PFE significantly inhibited (60.4 ± 8.3%) contractile responses of histamine and produced significant inhibition (56-79%: p 0.001) of mast cell degranulation. Conclusion: PFE has anti-asthmatic, antihistaminic, and mast cell stabilization effect making it useful in traditional asthma management.

show abstract

“…Studies demonstrated that, NO levels in exhaled air were increased 30 min after OVA challenge to sensitized animals, with a concomitant increase in airway constriction (Smith Broadley, 2007). This suggests that iNOS-derived NO promotes bronchial hyperactivity and eosinophil infiltration in the airways as a consequence of Th1/Th2 imbalance (Nevin Broadley, 2002).…”

Section: Discussionmentioning

confidence: 99%

Anti-asthmatic potential of chrysin on ovalbumin-induced bronchoalveolar hyperresponsiveness in rats

Wadibhasme

Ghaisas

Thakurdesai

2011

Pharmaceutical Biology

View full text Add to dashboard Cite

Optimisation of the sensitisation conditions for an ovalbumin challenge model of asthma

Cited by 40 publications

References 43 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

Anti-asthmatic property and possible mode of activity of an ethanol leaf extract ofPolyscias fruticosa

Anti-asthmatic potential of chrysin on ovalbumin-induced bronchoalveolar hyperresponsiveness in rats

Contact Info

Product

Resources

About