宾夕法尼亚代写论文:慢性气道炎症

2017-04-14 00:31

哮喘的慢性气道炎症是独特的，气道壁是由辅助性T淋巴细胞（TH）浸润型2型，嗜酸性粒细胞、巨噬细胞和肥大细胞。此外，急性发作期炎症可能在病情加重时观察到，嗜酸性粒细胞增多，有时嗜中性粒细胞增多（巴尼斯1995）。支气管哮喘的主要异常是气道平滑肌收缩，通过自主神经系统的副交感神经科或刺激引起（ANS）或过敏反应介质，如组胺、前列腺素、激肽和白三烯（Tortora和格拉鲍夫斯基，1996）。先前遇到抗原的肥大细胞与IgE抗体（过敏原特异性免疫球蛋白）。再次暴露于过敏原后，IgE抗体是“桥接”的。这导致肥大细胞脱颗粒，释放过敏反应介质（组胺）。白三烯和组胺会引起支气管平滑肌痉挛。血管扩张，毛细血管通透性增加，T辅助细胞和嗜酸性粒细胞的吸引力也发生，设置延迟或晚期相位响应的场景。这发生在不同的时间接触过敏原后，可能是夜间（响et al，2003）。ATIn气道，潜在的哮喘发作开始的初始敏感事件级联吸入抗原（过敏原），从而刺激诱导Th2细胞释放的细胞因子如IL-4、IL-5（图1）。这些细胞因子，反过来，由B细胞促进IgE的产生，肥大细胞生长（IL-4），和生长和嗜酸性粒细胞活化（IL-5）。随后的IgE介导的吸入变应原引起的反应，急性反应和后期反应。
宾夕法尼亚代写论文:慢性气道炎症
The chronic airway inflammation of asthma is unique in that the airway wall is infiltrated by T-lymphocytes of the T-helper (Th) type 2 phenotype, eosinophils, macrophages/monocytes and mast cells. In addition, an ‘acute-on-chronic’ inflammation may be observed during exacerbations, with an increase in eosinophils and sometimes neutrophils (Barnes 1995). The main abnormality in bronchial asthma is airway smooth muscle contraction, caused by either stimulation of the parasympathetic division of the autonomic nervous system (ANS) or mediators of allergic reactions, e.g. histamine, prostaglandins, kinins and leukotrienes (Tortora and Grabowski, 1996). Previously encountered antigens prime the mast cells with IgE antibodies (allergen-specific immunoglobulins). Following re-exposure to the allergen, the IgE antibodies are ‘bridged’. This results in degranulation of mast cells, and the release of allergic response mediators (histamine). Leukotrienes and histamine will often cause spasm of the bronchial smooth muscle. Vasodilation, increased permeability of capillaries and attraction of T helper cells and eosinophils also occur, setting the scene for the delayed or late-phase response. This happens at varying times after exposure to the allergen and may be nocturnal (Rang et al, 2003).ATIn the airways, the cascade of events underlying an asthmatic attack begins the initial sensitization to inhaled antigens (allergens), which stimulate induction of TH2-type cells that release cytokines such as IL-4 and IL-5 (Fig. 1). These cytokines, in turn, promote IgE production by B cells, growth of mast cells (IL-4), and growth and activation of eosinophils (IL-5). Subsequent IgE-mediated reaction to inhaled allergens elicits an acute response and a late-phase reaction.

• 上一篇：宾夕法尼亚作业代写：灵活和创造性
• 下一篇：宾夕法尼亚代写Essay:光谱学校