Recent advances in pathogenesis of allergic alveolitis

Recent advances in pathogenesis of allergic alveolitis
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过敏性肺泡炎发病机制的最新进展

DOI:
--
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发表时间:
1990
影响因子:
6.1
通讯作者:
J. Salvaggio
J. Salvaggio
中科院分区:
医学2区
文献类型:
--
作者:
J. Salvaggio

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上述动物模型研究似乎表明,AA的发展是一系列复杂的免疫特异性事件的结果,包括初始致敏,以及由一系列遗传决定的免疫刺激事件引起的肉芽肿性炎症反应的发展。通过前面讨论的几种方法调节实验性肉芽肿病变可能为人类AA的发病率和临床病程以及未来治疗和/或预防该疾病提供一些重要线索。例如,在先前讨论的动物模型中,慢性暴露于雾化抗原导致特异性“脱敏”,在人类中,这种反复的挑战可能会被改进到诱导类似的长时间不应期和肺部炎症减少的程度。具有抗脂氧合酶活性的抑制剂(如纳扎特仑和去二氢木胍酸)和环孢素显著抑制小鼠超敏性肺肉芽肿的实验证明,也可能为研究这些药物在人类肉芽肿性肺部疾病的实验治疗中打开大门。很明显,更好地了解人类的这些机制可以提供重要的信息,以增加我们对慢性肉芽肿性肺部疾病可能的预防、调节和治疗的理解。
The animal-model studies discussed above appear to suggest that AA develops as the result of a complex series of immunologically specific events, involving initial sensitization, and the development of granulomatous inflammatory response by a series of genetically determined immunostimulatory events. Modulation of experimental granulomatous lesions by several of the means previously discussed may offer some important clues to the incidence and clinical course of AA in man and to future therapy and/or prevention of the disease. For example, in the animal models discussed previously in which chronic exposure to aerosolized antigen resulted in specific 'desensitization' it is possible that such repeated challenge in man may be refined to the point of inducing similar lengthy refractory periods and a decrease in pulmonary inflammation. The demonstration that hypersensitivity-type pulmonary granulomas in mice are markedly suppressed by inhibitors possessing antilipoxygenase activity, such as nafazatrom and nordihydroguairetic acid and by cyclosporine, may also open the door to investigation of such agents in the experimental treatment of granulomatous pulmonary diseases in man. It is obvious that a better understanding of these mechanisms in man can provide important information to increase our understanding of the possible prevention, modulation, and therapy of chronic granulomatous pulmonary disease.
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