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Procoagulant activity of human alveolar macrophages: Different expression in patients with lung cancer
Author(s) -
Semeraro Nicola,
De Lucia Onofrio,
Lattanzio Angela,
Montemurro Pasqualina,
Giordano Domenico,
Loizzi Michele,
Carpagnano Francesco
Publication year - 1986
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910370409
Subject(s) - bronchoalveolar lavage , pathology , lung cancer , basal (medicine) , lung , macrophage , medicine , lewis lung carcinoma , in vitro , immunology , cancer , chemistry , biochemistry , metastasis , insulin
Mononuclear phagocytes, an integral part of the lymphoreticular infiltrate of many malignant tissues, might contribute to tumor‐associated fibrin deposition through the production of procoagulant activity (PCA). We have studied the PCA of human alveolar macrophages in 28 patients with primary lung cancer and in 9 control subjects. Alveolar macrophages (> 97% esterase positive) were isolated from bronchoalveolar lavage fluids by adherence onto plastic. PCA was evaluated by a one‐stage clotting assay immediately after isolation (basal PCA) and after incubation ( hr at 37°C) in the absence and in the presence of endotoxin. Cells from control subjects had low basal PCA (3.9 ± 1.0 units/5 × 10 4 cells) but, upon exposure to endotoxin, they displayed a 5‐ to 16‐fold increase in PCA. In patients, different patterns of PCA were observed. In the 8 patients in whom lavage had been carried out on the contralateral side to the neoplasm, alveolar macrophages behaved essentially like those from controls. In contrast, in the 20 patients in whom macrophage populations close to the site of the tumor were examined, PCA was abnormal in many respects. ± 12 of these, alveolar macrophages had basal PCA comparable to or somewhat lower than control cells, but exhibited a poor procoagulant response when incubated in vitro in the presence of endotoxin. Alveolar macrophages from the remaining 8 patients expressed far higher levels of basal PCA than control cells (25.1 ± 5.9 units as compared to 3.9 ± 1.0 units/5 × 10 4 cells). These cells retained their ability to respond to endotoxin in vitro with a 3‐fold increase in PCA. In all instances, alveolar macrophage PCA had the characteristics of tissue factor. These data suggest that the presence of primary lung cancer may moduate the expression of PCA in alveolar macrophages close to the tumor site. PCA might be useful to better characterize the functional state of macrophages near the tumor.