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首页> 外文期刊>Pulmonary pharmacology & therapeutics >Rat models of asthma and chronic obstructive lung disease.
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Rat models of asthma and chronic obstructive lung disease.

机译:哮喘和慢性阻塞性肺疾病的大鼠模型。

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摘要

The rat has been extensively used to model asthma and somewhat less extensively to model chronic obstructive pulmonary disease (COPD). The features of asthma that have been successfully modeled include allergen-induced airway constriction, eosinophilic inflammation and allergen-induced airway hyperresponsiveness. T-cell involvement has been directly demonstrated using adoptive transfer techniques. Both CD4+ and CD8+ T cells are activated in response to allergen challenge in the sensitized rat and express Thelper2 cytokines (IL-4, IL-5 and IL-13). Repeated allergen exposure causes airway remodeling. Dry gas hyperpnea challenge also evokes increases in lung resistance, allowing exercise-induced asthma to be modeled. COPD is modeled using elastase-induced parenchymal injury to mimic emphysema. Cigarette smoke-induced airspace enlargement occurs but requires months of cigarette exposure. Inflammation and fibrosis of peripheral airways is an important aspect of COPD that is less well modeled. Novel approaches to the treatment of COPD have been reported including treatments aimed at parenchymal regeneration.
机译:该大鼠已被广泛地用于哮喘的模型化,而被广泛地用于慢性阻塞性肺疾病(COPD)的模型化。已成功建模的哮喘特征包括过敏原诱发的气道收缩,嗜酸性粒细胞炎症和过敏原诱发的气道高反应性。使用过继转移技术已经直接证明了T细胞的参与。在致敏大鼠中,CD4 +和CD8 + T细胞均响应变应原激发而激活,并表达Thelper2细胞因子(IL-4,IL-5和IL-13)。反复接触过敏原会导致气道重塑。干气高通气激发也引起肺阻力增加,从而可以模拟运动诱发的哮喘。使用弹性蛋白酶诱导的实质损伤模拟肺气肿对COPD进行建模。香烟会引起烟雾扩散,但需要几个月的香烟暴露时间。周围呼吸道的炎症和纤维化是COPD的重要方面,其建模尚不完善。已经报道了治疗COPD的新方法,包括针对实质再生的治疗。

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