Experimental pleural effusion as a manifestation of delayed hypersensitivity to tuberculin PPD.
Experimental pleural effusion as a manifestation of delayed hypersensitivity to tuberculin PPD.
复制标题
实验性胸腔积液是对结核菌素 PPD 迟发型过敏的表现。
作者：
J. Allen;M. Apicella
有证据表明，在没有结核菌感染的情况下，豚鼠的胸腔积液可能是由对 PPD 过敏引起的。这种反应与来自免疫动物的细胞的转移表明了迟发型超敏反应的主要作用，并证明了这种形式的超敏反应在体内的额外生理效应。与非特异性化学损伤引起的渗出液相比，这些渗出液中蛋白质浓度的差异与由这种超敏反应引起的渗出液中大分子运动的控制差异相一致。利用致敏供体肺的体外培养进行的研究表明，在过敏反应期间释放的可溶性介质在诱导胸腔积液中发挥作用，因此表明此类介质在迟发性过敏的体内表现中的重要性。
Evidence is presented that pleural effusions in guinea pigs may be induced by hypersensitivity to PPD in the absence of infection with tuberculous organisms. Transfer of this reaction with cells from immunized animals indicates a predominant role of the delayed type of hypersensitivity, and documents an additional physiologic effect of this form of hypersensitivity reaction in vivo. Differences found in the protein concentrations of these effusions are compatible with differences in control of macromolecular movement in effusions induced by this hypersensitivity reaction, when compared with effusions resulting from nonspecific chemical injury. Studies utilizing in vitro incubations of lungs from sensitized donors indicate a role of soluble mediators released during the hypersensitivity reaction in the induction of pleural effusions, and thus suggest the importance of such mediators in in vivo manifestations of delayed hypersensitivity.