Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins.

Abstract

Biochemical analyses of bronchoalveolar lavage (BAL) supernatants of sheep treated with weekly intratracheal instillations (for 6 months) of saline, 2 mg, or 128 mg of asbestos (chrysotile B; UICC) were performed. Our results showed that proteins (either total or its various components) and phospholipase A2 activity were unchanged in the low exposure group as compared to controls. However, in the high exposure group, with histopathological evidence of early asbestosis, there were significant increases in total proteins, albumin, a2-globulin, f3-and y-globulins as well as phospholipase A2 activity of BAL fluid. Prostaglandin E2 activity was significantly increased in both low and high dose groups. These changes in protein and lipid components of BAL following asbestos exposure constitute early indices of lung inflammatory reactions which may contribute to the development of asbestosis.

Cyclooxygenase‐ and lipoxygenase‐derived eicosanoids in bronchoalveolar lavage fluid from patients with scleroderma lung disease: An imbalance between proinflammatory and antiinflammatory lipid mediators

“…The results of our study are further supported by reports that alveolar macrophages from patients with interstitial lung fibrosis, including those with IPF and SLD, produce increased amounts of PGE 2 , and the increased production of PGE 2 seen in alveolar macrophages from patients with interstitial lung disease has been considered to be a protective mechanism (46, 47). Studies based on different animal models of lung fibrosis also show that exposure of lung macrophages to extrinsic factors, including bleomycin, results in increased production of PGE 2 (48–50). Finally, our data indicate the possibility that despite elevated levels of PGE 2 , there may be an insufficient response to PGE 2 .…”