4.5 Article

Effect of bronchial thermoplasty on structural changes and inflammatory mediators in the airways of subjects with severe asthma

期刊

RESPIRATORY MEDICINE
卷 150, 期 -, 页码 165-172

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W B SAUNDERS CO LTD
DOI: 10.1016/j.rmed.2019.03.005

关键词

Bronchial thermoplasty; Severe asthma; Airway smooth muscle; Airway remodeling; Airway nerves; Inflammatory mediators

资金

  1. Richard and Edith Strauss Foundation
  2. Banyu Fellowship Program - Banyu Life Science Foundation International

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Background: Bronchial thermoplasty (BT) is a novel technique used in the treatment of subjects with severe refractory asthma. Radiofrequency is provided to airway walls during bronchoscopy in order to reduce airway remodeling. Several clinical studies have reported an improvement in subjects' symptoms following BT. However, how BT affects the airway architectures and inflammatory mediators in the airways has not been yet fully elucidated. Methods: Fourteen subjects with severe asthma were recruited in this study according to the criteria of ATS severe asthma definition. The study subjects undertook bronchial biopsy during the bronchoscopy procedure at baseline and 6 weeks after the initial BT treatment. The obtained samples were stained with antibodies for alpha-smooth muscle actin (alpha-SMA); protein gene product (PGP) 9.5, a specific nerve marker; von Willebrand factor (vWF), a marker for blood vessels; interleukin-17A (IL-17A) and transforming growth factor-beta 1 (TGF-beta 1). Results: The expression of alpha-SMA and PGP9.5 were significantly reduced post-BT. There was no significant difference in the number of blood vessels between baseline and post-BT. In addition, BT did not affect the production of IL-17A and TGF-beta 1 in the airways. The changes in the expression of alpha-SMA and PGP9.5 had no significant correlation with the improvement of pulmonary function. Conclusion: and Clinical Relevance: This study suggests that BT reduces airway smooth muscle mass and the airway innervation without affecting vasculature and the production of inflammatory mediators in the airways of subjects with severe asthma.

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