当前位置: X-MOL 学术Int. Arch. Allergy Immunol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
The Effect of Bronchoconstriction by Methacholine Inhalation in a Murine Model of Asthma.
International Archives of Allergy and Immunology ( IF 2.8 ) Pub Date : 2020-08-13 , DOI: 10.1159/000509606
Yoshito Miyata 1 , Shin Ohta 2 , Akihiko Tanaka 1 , Ayaka Kashima 1 , Hiromitsu Suganuma 1 , Tomoki Uno 1 , Haruna Sato 1 , Hitomi Ida 1 , Tomoyuki Kimura 1 , Megumi Jinno 1 , Kuniaki Hirai 1 , Tetsuya Homma 1 , Mayumi Yamamoto 1 , Yoshio Watanabe 1 , Shintaro Suzuki 1 , Hironori Sagara 1
Affiliation  

Introduction: Bronchoconstriction was recently shown to cause airway remodeling and induce allergic airway inflammation in asthma. However, the mechanisms how mechanical stress via bronchoconstriction could induce airway inflammation and remodeling remain unclear. Objective: We investigated the effect of bronchoconstriction induced by methacholine inhalation in a murine model of asthma. Methods: BALB/c female mice were sensitized and challenged with ovalbumin (OVA), followed by treatment with methacholine by a nebulizer twice a day for 7 days. Twenty-four hours after the last methacholine treatment, the bronchoalveolar lavage fluid (BALF) and lung tissues were collected. The BALF was analyzed for total and differential cell counts and cytokine levels. The lung tissues were analyzed for goblet cell metaplasia, thickness of the smooth muscle, and lung fibrosis. The expression of cytokines in the lung was also examined. Results: OVA sensitization and challenge induced infiltration of total cells, macrophages, and eosinophils in the BALF along with goblet cell metaplasia and increased airway smooth muscle hypertrophy. Seven days after the last OVA challenge, untreated mice achieved reduction in airway inflammation, while methacholine maintained the number of BALF total cells, macrophages, and eosinophils. The percentage of goblet cells and the thickness of airway smooth muscle were also maintained by methacholine. Moreover, the treatment of methacholine induced the expression of transforming growth factor (TGF)-β in the lung. This result indicates that the production of TGF-β is involved in induction of airway remodeling caused by bronchoconstriction with methacholine. Conclusions: Repeated bronchoconstriction caused by methacholine inhalation elicited allergic airway inflammation and airway remodeling.
Int Arch Allergy Immunol


中文翻译:

吸入甲胆碱对哮喘小鼠模型的支气管收缩作用。

简介:最近发现支气管收缩可引起哮喘的气道重塑并引起过敏性气道炎症。但是,支气管收缩引起的机械应力如何引起气道炎症和重塑的机制仍不清楚。目的:我们研究了吸入乙酰甲胆碱引起的支气管收缩在小鼠哮喘模型中的作用。方法:将BALB / c雌性小鼠致敏并用卵清蛋白(OVA)攻击,然后每天两次用雾化器用甲胆碱治疗,持续7天。最后一次乙酰甲胆碱治疗后二十四小时,收集了支气管肺泡灌洗液(BALF)和肺组织。分析了BALF的总细胞数和差异细胞数以及细胞因子水平。分析了肺组织的杯状细胞化生,平滑肌厚度和肺纤维化。还检查了肺中细胞因子的表达。结果:OVA致敏和攻击诱导了BALF中总细胞,巨噬细胞和嗜酸性粒细胞的浸润以及杯状细胞化生和气道平滑肌肥大。在最后一次OVA攻击后7天,未经治疗的小鼠气道炎症减轻,而乙酰甲胆碱维持BALF总细胞,巨噬细胞和嗜酸性粒细胞的数量。乙酰甲胆碱也能维持杯状细胞的百分比和气道平滑肌的厚度。此外,乙酰甲胆碱的治疗诱导了肺中转化生长因子(TGF)-β的表达。该结果表明,TGF-β的产生参与了由乙酰甲胆碱引起的支气管收缩引起的气道重塑。结论:乙酰甲胆碱吸入引起的反复支气管收缩引起过敏性气道炎症和气道重塑。
Int Arch过敏免疫
更新日期:2020-08-14
down
wechat
bug