LOSS OF LYMPHOCYTE MODULATORY CONTROL BY SURFACTANT LIPID EXTRACTS FROM ACUTE HYPERSENSITIVITY PNEUMONITIS - COMPARISON WITH SARCOIDOSIS AND IDIOPATHIC PULMONARY FIBROSIS

Surfactant components are recognized to exert a regulatory control on lymphocytes in physiological conditions, as testified by in vitro stud ies. However, what happens following lung injury has not been establis hed. As surfactant composition is altered in interstitial lung disease s, this work was carried out to compare the modulatory impact of norma l human alveolar fluids on lymphocyte proliferation, with that from in flammatory lung diseases which are characterized by distinct patterns of immunologically-mediated alterations (i.e. sarcoidosis, acute hyper sensitivity pneumonitis, idiopathic pulmonary fibrosis). Thymidine inc orporation of allogeneic normal human blood lymphocytes was studied in the presence of total alveolar fluids or lipid extracts from 37 subje cts, and phytohaemagglutinin (PHA) as T-cell mitogen. The results show that: 1) total alveolar fluids and lipid extracts from normal subject s share a concentration-dependent suppressive activity on T-cell proli feration; 2) total alveolar fluids from diseased patients have lost th is property, either by a lack of suppressive activity (i.e. idiopathic pulmonary fibrosis) or even by enhanced activity (i.e. sarcoidosis an d hypersensitivity pneumonitis); 3) lipid extracts from diseased patie nts still retain the suppressive activity of normal subjects, except f or hypersensitivity; and 4) an imbalance in surfactant phospholipids w ith an increase in the inducers to suppressors ratio is more likely to explain this alteration in hypersensitivity pneumonitis than changes in total lipid content. In conclusion, alveolar lipid extracts from ac ute hypersensitivity pneumonitis have lost the modulatory control norm ally exerted by surfactant lipids on lymphocyte proliferation in vitro . This alteration may contribute to the invasion of the lung by lympho cytes in acute hypersensitivity pneumonitis in vivo.