Allergic rhinitis: not purely a histamine-related disease
Allergic rhinitis: not purely a histamine-related disease
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DOI：
10.1034/j.1398-9995.2000.00802.x
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发表时间：
2000-01-01
期刊：
影响因子：
12.4
通讯作者：
Dokic, D
中科院分区：
文献类型：
--
作者：
Howarth, PH;Salagean, M;Dokic, D
变应性鼻炎是一种鼻黏膜炎症性疾病，以鼻痒、打喷嚏、前鼻分泌物和鼻塞为典型症状。这些症状是由介质与鼻子内的神经、血管和腺体结构之间的相互作用引起的。鼻痒、打喷嚏和鼻溢症主要是神经性的，而鼻塞主要是血管的。鼻活检研究显示，在季节性和常年性变应性鼻炎中，固有层和上皮中的嗜酸性粒细胞聚集，组织和细胞表面的嗜碱性粒细胞增加。这些细胞处于激活状态。在上皮内，发现诱导T细胞活化的肥大细胞、T细胞和朗格汉斯细胞的数量增加。这些细胞的积累可能与上皮细胞本身产生的趋化因子和细胞因子有关。因此，组织细胞。招募是由激活的肥大细胞、T细胞和上皮细胞协调的，招募的组织嗜酸性粒细胞也通过自分泌机制促进其在该部位的持续存在。肥大细胞产生一系列的介质，包括组胺、类胰蛋白酶、白三烯和前列腺素。嗜碱性细胞也会产生组胺。嗜酸性粒细胞和嗜碱性粒细胞促进组织内白三烯的合成。组胺鼻腔注射会引起鼻痒、打喷嚏、鼻溢以及鼻塞，从而重现过敏性鼻炎的所有症状。这些作用主要是由H-1受体介导的，而H-1受体拮抗剂是一种重要的治疗方法。组胺在这些受体上的拮抗作用可减少约40%-50%的症状，对神经中介反应的影响最大。因此，组胺是过敏性鼻炎的主要媒介，但不是唯一的因素。鼻腔注射白三烯、前列腺素或激动素与鼻塞的发生有关。这些介质主要作用于鼻腔血管系统，在这方面，白三烯是有效的介质。白三烯还会诱导血浆蛋白渗出，从而导致前鼻腔分泌物。使用组合产品的研究表明，修改白三烯和组胺的效果在缓解鼻部症状方面具有互补作用，表明这两种介质与疾病表现相关。
Allergic rhinitis is an inflammatory disorder of the nasal mucosa typified by the symptoms of nasal itch, sneeze, anterior nasal secretions, and nasal blockage. These symptoms arise from the interaction between mediators and neural, vascular, and glandular structures within the nose. Nasal itch, sneezes, and rhinorrhoea are predominantly neural in origin, while nasal obstruction is predominantly vascular. Nasal biopsy studies show accumulation of eosinophils within the lamina propria and epithelium and an increase in tissue and cell surface basophils in both seasonal and perennial allergic rhinitis. These cells are in an activated state. Within the epithelium, increased numbers of mast cells, T cells and Langerhans' cells, which induce T-cell activation, are found. The accumulation of these cells can be linked to chemokine and cytokine generation by the epithelial cells themselves. Thus, the tissue cell. recruitment is orchestrated by activated mast cells, T cells, and epithelial cells, with the recruited tissue eosinophils also contributing to their persistence at this site through autocrine mechanisms. Mast cells generate an array of mediators including histamine, tryptase, leukotrienes, and prostaglandins. Histamine is also generated by basophils. Eosinophils and basophils contribute to the leukotriene synthesis within the tissue. Histamine nasal insufflation induces nasal itch, sneeze, and rhinorrhoea as well as nasal blockage, thereby reproducing all the symptoms of allergic rhinitis. These effects are primarily mediated by H-1-receptors, and H-1-receptor antagonists are a prominent treatment. Antagonism of histamine at these receptors reduces symptoms by about 40-50%, with the greatest effect on the neurally mediated responses. Thus, histamine is a major mediator of allergic rhinitis, but not the sole contributor. Nasal insufflation with leukotrienes, prostaglandins, or kinins is associated with the development of nasal blockage. These mediators act primarily on the nasal vasculature and, in this respect, leukotrienes are potent mediators. Leukotrienes also induce plasma protein exudation, which contributes to the anterior nasal secretions. Studies with combination products have suggested that modifying the effects of both leukotrienes and histamine has complementary effects in relieving nasal symptoms, indicating that both these mediators are relevant to disease expression.