Bronchoconstriction - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies


The Experts below are selected from a list of 225 Experts worldwide ranked by ideXlab platform

Reinoud Gosens – 1st expert on this subject based on the ideXlab platform

  • acetylcholine beyond Bronchoconstriction roles in inflammation and remodeling
    Trends in Pharmacological Sciences, 2015
    Co-Authors: Loes E M Kistemaker, Reinoud Gosens


    Acetylcholine is the primary parasympathetic neurotransmitter in the airways, where it not only induces Bronchoconstriction and mucus secretion, but also regulates airway inflammation and remodeling. In this review, we propose that these effects are all primarily mediated via the muscarinic M 3 receptor. Acetylcholine promotes inflammation and remodeling via direct effects on airway cells, and via mechanical stress applied to the airways sequential to Bronchoconstriction. The effects on inflammation and remodeling are regulated by both neuronal and non-neuronal acetylcholine. Taken together, we believe that the combined effects of anticholinergic therapy on M 3 -mediated Bronchoconstriction, mucus secretion, inflammation, and remodeling may account for the positive outcome of treatment with these drugs for patients with chronic pulmonary obstructive disease (COPD) or asthma.

  • Bronchoconstriction induces tgf β release and airway remodelling in guinea pig lung slices
    PLOS ONE, 2013
    Co-Authors: Tjitske A Oenema, Harm Maarsingh, Marieke Smit, Geny M M Groothuis, Herman Meurs, Reinoud Gosens


    Airway remodelling, including smooth muscle remodelling, is a primary cause of airflow limitation in asthma. Recent evidence links Bronchoconstriction to airway remodelling in asthma. The mechanisms involved are poorly understood. A possible player is the multifunctional cytokine TGF-β, which plays an important role in airway remodelling. Guinea pig lung slices were used as an in vitro model to investigate mechanisms involved in Bronchoconstriction-induced airway remodelling. To address this aim, mechanical effects of bronchoconstricting stimuli on contractile protein expression and TGF-β release were investigated. Lung slices were viable for at least 48 h. Both methacholine and TGF-β1 augmented the expression of contractile proteins (sm-α-actin, sm-myosin, calponin) after 48 h. Confocal fluorescence microscopy showed that increased sm-myosin expression was enhanced in the peripheral airways and the central airways. Mechanistic studies demonstrated that methacholine-induced Bronchoconstriction mediated the release of biologically active TGF-β, which caused the increased contractile protein expression, as inhibition of actin polymerization (latrunculin A) or TGF-β receptor kinase (SB431542) prevented the methacholine effects, whereas other bronchoconstricting agents (histamine and KCl) mimicked the effects of methacholine. Collectively, Bronchoconstriction promotes the release of TGF-β, which induces airway smooth muscle remodelling. This study shows that lung slices are a useful in vitro model to study mechanisms involved in airway remodelling.

M. Hermel – 2nd expert on this subject based on the ideXlab platform

  • Influence of atrial natriuretic peptide, brain natriuretic peptide and urodilatin on the histamine-induced Bronchoconstriction in the conscious guinea pig
    InflammoPharmacology, 1998
    Co-Authors: M. Hermel


    The influence of human atrial natriuretic peptide (ANP) and of two related peptides, human brain natriuretic peptide (BNP) and urodilatin (URO) on the Bronchoconstriction induced by inhalation of histamine in conscious, non-anaesthetized guinea pigs was tested. Changes in lung function were registered using two independent methods, one operating in a closed body-plethysmographic system, the other in an open system based on the time lag of air flow curves. The peptides were infused (0.25 ml/min) into the jugular vein for a period from 10 min before until 15 min after the histamine inhalation. ANP displayed virtually no effect on the Bronchoconstriction. URO showed some inibition at 1280ng kg^−1 min^−1, but not at lower doses. BNP (640ng kg^−1 min^−1) inhibited the Bronchoconstriction markedly for the total registration period. It can be concluded from these results that BNP exerts bronchoprotective effects in the conscious guinea pig, which are superior to those of ANP or URO.

Paul M Obyrne – 3rd expert on this subject based on the ideXlab platform

  • the interaction between Bronchoconstriction and cough in asthma
    Thorax, 2017
    Co-Authors: Imran Satia, Huda Badri, Mark Woodhead, Stephen J. Fowler, Paul M Obyrne, Jaclyn A. Smith


    Variable airflow obstruction is a pathophysiological hallmark of asthma; however, the interactions between acute Bronchoconstriction and the cough reflex are poorly understood. We performed a randomised, single-blind, placebo-controlled, crossover study to investigate the interaction between Bronchoconstriction and cough in asthma. Capsaicin was administered to evoke coughs and methacholine to induce Bronchoconstriction. We demonstrated that acute Bronchoconstriction increased capsaicin-evoked coughs, which improved as airway calibre spontaneously resolved. However, capsaicin-evoked coughing had no impact on methacholine-induced Bronchoconstriction. This study provides evidence that Bronchoconstriction increases the activation of capsaicin-responsive airway nerves, but the precise mechanisms and mediators involved require further evaluation. Trial registration number ISRCTN14900082.

  • effect of ciclesonide dose and duration of therapy on exercise induced Bronchoconstriction in patients with asthma
    The Journal of Allergy and Clinical Immunology, 2006
    Co-Authors: Padmaja Subbarao, Mylinh Duong, Ellinor Adelroth, Joceline Otis, G Obminski, Mark D Inman, Soren Pedersen, Paul M Obyrne


    Effect of ciclesonide dose and duration of therapy on exercise-induced Bronchoconstriction in patients with asthma.

  • evidence for mast cell activation during exercise induced Bronchoconstriction
    European Respiratory Journal, 1998
    Co-Authors: Siobhan Osullivan, Paul M Obyrne, A Roquet, Barbro Dahlen, F Larsen, Anders Eklund, Maria Kumlin, S E Dahlen


    Controversy remains about the causative mediators in the bronchoconstrictive response to exercise in asthma. This study examined whether mast cell activation is a feature of exercise-induced Bronchoconstriction by measuring urinary metabolites of mast cell mediators. Twelve nonsmoking subjects with mild asthma and a history of exercise-induced Bronchoconstriction exercised on a stationary bicycle ergometer for 5 min at 80% maximum work load. Pulmonary function was monitored and urine was collected before and 30 and 90 min after the provocation. The urinary concentrations of the mast cell markers 9alpha,11beta-prostaglandin (PG)F2 and Ntau-methylhistamine, as well as leukotriene E4 (LTE4) were determined by immunoassay. Seven of the 12 subjects (responders) experienced Bronchoconstriction (>15% fall in the forced expiratory volume in one second) following exercise, whereas the pulmonary function of the remaining five subjects (nonresponders) remained stable. The urinary excretion (mean+/-SE) of 9alpha,11beta-PGF2 in the responders increased significantly compared with the nonresponders at 30 (77.1+/-14.4 versus 37.2+/-5.6; p<0.05) and 90 min (79.3+/-8.6 versus 40.4+/-8.5, p<0.05) after exercise challenge. The urinary excretion of Ntau-methylhistamine and LTE4 was not significantly different between the two groups at 30 or 90 min after exercise. The findings represent the first documentation of increased urinary levels of 9alpha,11beta-prostaglandin F2 in adults following exercise challenge and provides clear evidence for mast cell activation during exercise-induced Bronchoconstriction in asthmatics.