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research
Procoagulant activity of bronchoalveolar lavage fluids taken from the site of tuberculous lesions
Authors
P R Narayanan
R Prabhakar
+3 more
P Selvaraj
N Venkataprasad
V K Vijayan
Publication date
1 January 1994
Publisher
'European Respiratory Society (ERS)'
Abstract
Procoagulant activity of bronchoalveolar lavage fluids taken from the site of tuberculous lesions. P. Selvaraj, N. Venkataprasad, V.K. Vijayan, R Prabhakar, P.R Narayanan. ©ERS Journals Ltd 1991. 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 cocultured 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
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oai:eprints.nirt.res.in:385
Last time updated on 15/06/2017