TY - JOUR
T1 - Correlation between PGE2 production and suppressor activity of alveolar macrophages from patients with interstitial lung diseases
AU - Fireman, E.
AU - Ben Efraim, S.
AU - Greif, J.
AU - Alguetti, A.
AU - Ayalon, D.
AU - Topilsky, M.
PY - 1988/6
Y1 - 1988/6
N2 - The suppressive activity of alveolar macrophages (AM) obtained from bronchoalveolar lavage (BAL), on PHA stimulation of autologous peripheral blood lymphocytes (APL) was evaluated. The effect on lymphocyte stimulation was evaluated by coculturing the AM and APL cells at a ratio of 1:1. PGE2 released by AM during the culture period was measured by a radioimmune assay. The patients included in the study were 11 cases with interstitial lung disease (ILD), 8 cases of lung cancer (CA), and 5 controls (CO). Addition of AM of patients from the CA group resulted in slight suppression of lymphocyte stimulation in 4 cases, slight enhancement in 3 cases and no effect in one case. AM from the CO group induced slight suppression in 4 out of 5 cases. AM from all 11 ILD cases exerted a significant high suppressive activity (65.6% ± 18.2 - P < 0.001 by comparison with the CO and CA groups). In ILD cases, a dichotomous pattern was found in regard to relation between high suppressive activity of AM and release of PGE2: in idiopathic pulmonary fibrosis (IPF) patients, high suppressive activity of AM (70.4% ± 15.4) correlated well with elevated secretion of PGE2: 3.58±0.26 ng/ml/105 cells (P < 0.02 compared to CO). AM from sarcoidosis patients suppressed PHA stimulation by 61.6% ± 19.3 but secreted only 0.357 ± 0.26 ng/ml/105 cells of PGE2 (P < 0.02 compared with the idiopathic pulmonary fibrosis group). Therefore, it seems that other factors, in addition to PGE2, might be involved in the suppressive activity of AM from interstitial lung diseases.
AB - The suppressive activity of alveolar macrophages (AM) obtained from bronchoalveolar lavage (BAL), on PHA stimulation of autologous peripheral blood lymphocytes (APL) was evaluated. The effect on lymphocyte stimulation was evaluated by coculturing the AM and APL cells at a ratio of 1:1. PGE2 released by AM during the culture period was measured by a radioimmune assay. The patients included in the study were 11 cases with interstitial lung disease (ILD), 8 cases of lung cancer (CA), and 5 controls (CO). Addition of AM of patients from the CA group resulted in slight suppression of lymphocyte stimulation in 4 cases, slight enhancement in 3 cases and no effect in one case. AM from the CO group induced slight suppression in 4 out of 5 cases. AM from all 11 ILD cases exerted a significant high suppressive activity (65.6% ± 18.2 - P < 0.001 by comparison with the CO and CA groups). In ILD cases, a dichotomous pattern was found in regard to relation between high suppressive activity of AM and release of PGE2: in idiopathic pulmonary fibrosis (IPF) patients, high suppressive activity of AM (70.4% ± 15.4) correlated well with elevated secretion of PGE2: 3.58±0.26 ng/ml/105 cells (P < 0.02 compared to CO). AM from sarcoidosis patients suppressed PHA stimulation by 61.6% ± 19.3 but secreted only 0.357 ± 0.26 ng/ml/105 cells of PGE2 (P < 0.02 compared with the idiopathic pulmonary fibrosis group). Therefore, it seems that other factors, in addition to PGE2, might be involved in the suppressive activity of AM from interstitial lung diseases.
KW - Alveolar macrophages
KW - Interstitial lung diseases
KW - PGE production
KW - PHA stimulation
KW - Suppressive activity
UR - http://www.scopus.com/inward/record.url?scp=0024026195&partnerID=8YFLogxK
U2 - 10.1016/0165-2478(88)90058-2
DO - 10.1016/0165-2478(88)90058-2
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AN - SCOPUS:0024026195
SN - 0165-2478
VL - 18
SP - 159
EP - 165
JO - Immunology Letters
JF - Immunology Letters
IS - 2
ER -
