Cultured human alveolar macrophages from smokers with lung cancer: resolution of factors that stimulate fibroblast proliferation, production of collagenase, or prostaglandin E2.
Marked connective tissue remodelling involves both destruction and repair in inflammatory lung diseases. Throughout the remodelling event, it was reasoned that alveolar macrophages may release substances similar to those produced by blood monocyte-macrophages that affect fibroblast functions, ie, the interleukin 1 family of monokines (or cytokines). We have examined human alveolar macrophage cultures obtained after bronchoalveolar lavage of freshly excised lungs from heavy smokers with bronchial carcinoma. Crude culture media contained fibroblast proliferative activity and collagenase- and PGE2- production-stimulating activity. The main peak of these biological activities was located around approximately 18 kilodaltons (kD) on gel filtration chromatography. Resolution of this peak by high performance liquid chromatography showed the presence of three distinct peaks, with quantitative and qualitative differences in biological activities. This suggests the presence of heterogeneous factors.
Dayer
J M
JM
Sundström
L
L
Polla
B S
BS
Junod
A F
AF
D002455:Cell Division; D015232:Dinoprostone; D005346:Fibroblast Growth Factors / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology; D006801:Humans; D008175:Lung Neoplasms / Q000473:pathology / Q000503:physiopathology*; D008264:Macrophages / Q000502:physiology*; D003012:Microbial Collagenase / Q000096:biosynthesis*; D011458:Prostaglandins E / Q000096:biosynthesis; D011650:Pulmonary Alveoli / Q000473:pathology; D012907:Smoking
D011458:Prostaglandins E; D005346:Fibroblast Growth Factors; D003012:Microbial Collagenase; D015232:Dinoprostone