PROCOAGULANT ACTIVITY OF BRONCHOALVEOLAR LAVAGE FLUIDS TAKEN FROM THESITE OF TUBERCULOUS LESIONS

Citation
P. Selvaraj et al., PROCOAGULANT ACTIVITY OF BRONCHOALVEOLAR LAVAGE FLUIDS TAKEN FROM THESITE OF TUBERCULOUS LESIONS, The European respiratory journal, 7(7), 1994, pp. 1227-1232
Citations number
33
Categorie Soggetti
Respiratory System
ISSN journal
09031936
Volume
7
Issue
7
Year of publication
1994
Pages
1227 - 1232
Database
ISI
SICI code
0903-1936(1994)7:7<1227:PAOBLF>2.0.ZU;2-7
Abstract
We wanted to determine the procoagulant activity (PCA) of bronchoalveo lar lavage fluids, in order to understand the macrophage-mediated lung injury at the site of tuberculous lesion. Alveolar lavage fluids take n from the site of a lesion (radiologically abnormal site (RAS)) and a n unaffected site (radiologically normal site (RNS)) of active pulmona ry 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/tendancies only. An increased PCA was seen in 4 out of 7 cell-free lavage supernatants of active-TB take n from the site of lesion (RAS), compared to only 1 out of 9 in inacti ve-TB. The PCA producing potential of the alveolar macrophages of RAS and RNS of active-TB patients was enhanced when the alveolar macrophag es 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 pr oduction. Peripheral blood monocytes and total mononuclear cells (mono cytes + 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 pr oduction of PCA by the alveolar macrophages, in collaboration with lym phocytes and other cells at the site of tuberculous lesions will resul t in fibrin formation. The deposition of fibrin in the alveoli may lea d to further lung injury.