Abstract

Asthma is the most common, long-lasting inflammatory airway disease that affects more than 10% of the world population. It is characterized by bronchial narrowing, airway hyperresponsiveness, vasodilatation, airway edema, and stimulation of sensory nerve endings that lead to recurring events of breathlessness, wheezing, chest tightness, and coughing. It is the main reason for global morbidity and occurs as a result of the weakening of the immune system in response to exposure to allergens or environmental exposure. In asthma condition, it results in the activation of numerous inflammatory cells like the mast and dendritic cells along with the accumulation of activated eosinophils and lymphocytes at the inflammation site. The structural cells such as airway epithelial cells and smooth muscle cells release inflammatory mediators that promote the bronchial inflammation. Long-lasting bronchial inflammation can cause pathological alterations, viz. the improved thickness of the bronchial epithelium and friability of airway epithelial cells, epithelium fibrosis, hyperplasia, and hypertrophy of airway smooth muscle, angiogenesis, and mucus gland hyperplasia. The stimulation of bronchial epithelial cell would result in the release of inflammatory cytokines and chemokines that attract inflammatory cells into bronchial airways and plays an important role in asthma. Asthma patients who do not respond to marketed antiasthmatic drugs needed novel biological medications to regulate the asthmatic situation. The present review enumerates various types of asthma, etiological factors, and in vivo animal models for the induction of asthma. The underlying pathological, immunological mechanism of action, the role of inflammatory mediators, the effect of inflammation on the bronchial airways, newer treatment approaches, and novel biological targets of asthma have been discussed in this review.

摘要

哮喘是最常见，持续时间很长的炎症性气道疾病，感染了全球10％以上的人口。它的特征是支气管变窄，气道反应过度，血管舒张，气道水肿和刺激感觉神经末梢，导致反复出现呼吸困难，喘息，胸闷和咳嗽。这是全球发病率的主要原因，并且是由于暴露于过敏原或环境而导致免疫系统减弱而发生的。在哮喘病中，它会导致许多炎症细胞（如肥大细胞和树突状细胞）的活化，以及活化的嗜酸性粒细胞和淋巴细胞在炎症部位的积聚。呼吸道上皮细胞和平滑肌细胞等结构性细胞释放出可促进支气管炎症的炎症介质。长期支气管炎症可引起病理改变，即。改善了支气管上皮的厚度和气道上皮细胞的脆性，上皮纤维化，增生以及气道平滑肌肥大，血管生成和粘液腺增生。支气管上皮细胞的刺激将导致炎症性细胞因子和趋化因子的释放，从而吸引炎症性细胞进入支气管气道并在哮喘中起重要作用。对市售的抗哮喘药物无反应的哮喘患者需要新的生物药物来调节哮喘病情。本综述列举了各种类型的哮喘，用于诱导哮喘的体内动物模型。在这篇综述中讨论了潜在的病理，免疫作用机制，炎症介质的作用，炎症对支气管气道的影响，较新的治疗方法以及哮喘的新生物学靶标。