Comparison of human bronchiolar smooth muscle responsiveness in vitro with histological signs of inflammation.

Jongste, J.C. de; Mons, H.; Strik, R. Van; Bonta, I. L.; Kerrebijn, K. F.

doi:10.1136/thx.42.11.870

Cited by 11 publications

(7 citation statements)

References 17 publications

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“…Obstructive airways diseases, such as asthma and COPD, are characterized by airway hyperresponsive- Hypercellular lung tissue (endothelial cells and type I pneumocytes) [6,23,32] Pulmonary hypertension [128] Augmented endothelium mediated vascular relaxation [6] Increased Ca 2+ sensitization of vascular smooth muscle [29] Reduced exercise tolerance [32] Reduced transendothelial macromolecule transport [120] Reduced pulmonary inflammation in response to LPS exposure [130] ness to inhaled and endogenous bronchoconstrictors [36], which is in part accompanied by contractile abnormalities of the airway smooth muscle [37][38][39][40]. Notably, caveolin-1 and caveolin-2 are abundant in airway smooth muscle (Fig.…”

Section: Caveolae and Caveolins In The Regulation Of Airway Tone Airwmentioning

confidence: 99%

Caveolae and Caveolins in the Respiratory System

Gosens¹,

Mutawe²,

Martin³

et al. 2008

CMM

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Caveolae are flask-shaped invaginations of the plasma membrane that are present in most structural cells. They owe their characteristic Omega-shape to complexes of unique proteins, the caveolins, which indirectly tether cholesterol and sphingolipid-enriched membrane microdomains to the cytoskeleton. Caveolins possess a unique scaffolding domain that anchors receptors, ion channels, second messenger producing enzymes, and effector kinases, thereby sequestering them to caveolae, and modulating cellular signaling and vesicular transport. The lungs express numerous caveolae and high levels of caveolins; therefore they likely play an important role in lung physiology. Indeed, recent and ongoing studies indicate important roles for caveolae and caveolins in the airway epithelium, airway smooth muscle, airway fibroblasts, airway inflammatory cells and the pulmonary vasculature. We review the role of caveolae and caveolins in lung cells and discuss their involvement in cellular signaling associated with asthma, COPD, lung cancer, idiopathic pulmonary fibrosis and pulmonary vascular defects.

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Section: Caveolae and Caveolins In The Regulation Of Airway Tone Airwmentioning

confidence: 99%

Caveolae and Caveolins in the Respiratory System

Gosens¹,

Mutawe²,

Martin³

et al. 2008

CMM

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“…There are few studies comparing the force-generating capacity of asthmatic airway smooth muscle with normal muscle (22)(23)(24)(25)(26)(27). At least one (25) showed increased constrictor sensitivity, but others showed normal or reduced contractile function.…”

Section: Functional Effects Of Airway Smooth Muscle Proliferation Andmentioning

confidence: 99%

Airway Smooth Muscle Growth in Asthma: Proliferation, Hypertrophy, and Migration

Bentley

Hershenson

2008

Proceedings of the American Thoracic Society

160

128

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Increased airway smooth muscle mass is present in fatal and nonfatal asthma. However, little information is available regarding the cellular mechanism (i.e., hyperplasia vs. hypertrophy). Even less information exists regarding the functional consequences of airway smooth muscle remodeling. It would appear that increased airway smooth muscle mass would tend to increase airway narrowing and airflow obstruction. However, the precise effects of increased airway smooth muscle mass on airway narrowing are not known. This review will consider the evidence for airway smooth muscle cell proliferation and hypertrophy in asthma, potential functional effects, and biochemical mechanisms.

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“…Asthmatics have a mixed hypersensitivity and hyper-reactivity to the acute bronchoconstrictor effects of inhaled histamine with a shift to the left and an increase in the slope of the log doseresponse curve (Snashall, 1987) and, in two recent studies, lung tissues from asthmatics was found to be hyper-reactive to spasmogens (De Jongste et al, 1987;Bai, 1990).…”

Section: Eosinophilia and Lung Hyper-responsivenessmentioning

confidence: 99%

The effects of drugs on Sephadex‐induced eosinophilia and lung hyper‐responsiveness in the rat

Spicer¹,

Baker²,

Hatt³

et al. 1990

British J Pharmacology

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Rats given an intravenous injection of Sephadex particles (0.5 mg of G200 in 1 ml of saline) on days 0, 2 and 5 had a blood eosinophilia which was maximal on day 7. On day 7, broncho‐alveolar lavage (BAL) fluids taken from the rats contained an increased number of eosinophils and fewer mononuclear cells but there was no change in the small number of neutrophils. In addition the rats were hyper‐sensitive to the increase in resistance to artificial respiration produced by 5‐hydroxytryptamine (5‐HT), given intravenously, with a shift to the left of the log dose‐response curve. Lung parenchymal strips, taken from the rats on days 6, 7 and 8, were hyper‐reactive to 5‐HT with an increase in slope of the log dose‐response curve. Compounds with a wide variety of activities were evaluated for their effects on the blood eosinophilia on day 7 when given before each injection of Sephadex. The eosinophilia was reduced by glucocorticosteroids, β‐adrenoceptor agonists, aminophylline, dapsone and phenidone. Dexamethasone, isoprenaline, dapsone and phenidone at doses that reduced the blood eosinophilia also reduced the changes in number of leucocytes in the BAL fluids and the hyper‐responsiveness to 5‐HT in vivo and in vitro, except that the effects of dapsone on the hyper‐sensitivity to 5‐HT in vivo did not reach significance. Aminophylline was the least effective of the drugs at reducing the blood eosinophilia and its effects on the other changes did not reach significance. Sodium cromoglycate reduced the BAL eosinophilia but had no effect on the other changes produced by Sephadex. The correlation coefficients between blood eosinophil numbers and reactivity to 5‐HT in vitro and sensitivity in vivo were r = 0.76, (n = 88; P > 0.001) and r = 0.53, (n = 61; P > 0.001) respectively. Doses of dexamethasone, isoprenaline, dapsone and phenidone that reduced the blood eosinophilia when given before each injection of Sephadex were inactive when given up to 8 h after the Sephadex. These data show an association between blood eosinophilia and hyper‐responsiveness of the lung. The blood eosinophilia in the rats was triggered within the first few hours of injecting the Sephadex and drugs have been identified which inhibit this trigger.

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Comparison of human bronchiolar smooth muscle responsiveness in vitro with histological signs of inflammation.

Cited by 11 publications

References 17 publications

Caveolae and Caveolins in the Respiratory System

Caveolae and Caveolins in the Respiratory System

Airway Smooth Muscle Growth in Asthma: Proliferation, Hypertrophy, and Migration

The effects of drugs on Sephadex‐induced eosinophilia and lung hyper‐responsiveness in the rat

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