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取自结核病变部位的支气管肺泡灌洗液的促凝活性。

Procoagulant activity of bronchoalveolar lavage fluids taken from the site of tuberculous lesions.

作者信息

Selvaraj P, Venkataprasad N, Vijayan V K, Prabhakar R, Narayanan P R

机构信息

Tuberculosis Research Centre, Indian Council of Medical Research, Madras.

出版信息

Eur Respir J. 1994 Jul;7(7):1227-32. doi: 10.1183/09031936.94.07071227.

Abstract

We wanted to determine the procoagulant activity (PCA) of bronchoalveolar lavage fluids, in order to understand the macrophage-mediated lung injury at the site of tuberculous lesion. Alveolar lavage fluids taken from the site of a lesion (radiologically abnormal site (RAS)) and an unaffected site (radiologically normal site (RNS)) of active pulmonary tuberculosis (TB) patients (n = 7) and inactive (cured) patients (n = 9) were studied for their PCA producing potential. The observed results were not significant using Mann-Whitney test, and thus all increases/decreases reported below are trends/tendencies only. An increased PCA was seen in 4 out of 7 cell-free lavage supernatants of active-TB taken from the site of lesion (RAS), compared to only 1 out of 9 in inactive-TB. The PCA producing potential of the alveolar macrophages of RAS and RNS of active-TB patients was enhanced when the alveolar macrophages were co-cultured with autologous peripheral blood lymphocytes under in vitro condition. Stimulation with purified protein derivative (PPD) of M. tuberculosis showed a variable (increased or decreased) PCA production. Peripheral blood monocytes and total mononuclear cells (monocytes+lymphocytes) of active-TB patients stimulated with or without PPD showed increased PCA production, compared with normal individuals and inactive-TB patients. The present study suggests that increased production of PCA by the alveolar macrophages, in collaboration with lymphocytes and other cells at the site of tuberculous lesions will result in fibrin formation. The deposition of fibrin in the alveoli may lead to further lung injury.

摘要

我们想要测定支气管肺泡灌洗液的促凝血活性(PCA),以便了解结核病灶部位巨噬细胞介导的肺损伤。对来自活动性肺结核(TB)患者(n = 7)和非活动性(治愈)患者(n = 9)的病灶部位(放射学异常部位(RAS))和未受影响部位(放射学正常部位(RNS))的肺泡灌洗液的PCA产生潜力进行了研究。使用曼-惠特尼检验观察到的结果无统计学意义,因此下面报告的所有增加/减少仅为趋势。与非活动性TB患者9份中的1份相比,7份来自活动性TB病灶部位(RAS)的无细胞灌洗上清液中有4份PCA增加。当肺泡巨噬细胞在体外条件下与自体外周血淋巴细胞共培养时,活动性TB患者RAS和RNS的肺泡巨噬细胞的PCA产生潜力增强。用结核分枝杆菌纯化蛋白衍生物(PPD)刺激显示PCA产生变化(增加或减少)。与正常个体和非活动性TB患者相比,无论有无PPD刺激,活动性TB患者的外周血单核细胞和总单核细胞(单核细胞+淋巴细胞)均显示PCA产生增加。本研究表明,在结核病灶部位,肺泡巨噬细胞与淋巴细胞和其他细胞协同作用,导致PCA产生增加,进而导致纤维蛋白形成。肺泡中纤维蛋白的沉积可能导致进一步的肺损伤。

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