Abstract
The cell surface proteins of human alveolar macrophages obtained from nonsmokers have been compared to those of alveolar macrophages obtained from smokers. Proteins of nonsmokers' alveolar macrophages surface labeled with 125I differed from those of smokers' alveolar macrophages, as shown by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Three major radiolabeled proteins with molecular weights of 183,000, 80,000, and 30,000 were identified in fresh smokers' cells. The major radiolabeled protein of nonsmokers' macrophages had an apparent molecular weight of ∼183,000. Affinity chromatography suggested the Mr 183,000 protein is a mannose receptor. In contrast, the molecular weight of the major radiolabeled protein of smokers' alveolar macrophages was ∼30,000; the Mr 183,000 protein was less prominent. When nonsmokers' alveolar macrophages were cultured in vitro before 125I labeling, the cell surface protein pattern changed to resemble that of smokers' alveolar macrophages; the Mr 183,000 protein could no longer be detected on the cell surface, whereas a Mr 80,000 protein was increased in quantity and a new Mr 30,000 protein was detected. Nonadherent macrophages showed similar changes in their surface-labeled proteins but also contained a new prominently labeled Mr 70,000 protein. Limited proteolysis peptide mapping with five different enzymes did not reveal any evidence of homology among the Mr 183,000, 80,000, 70,000, and 30,000 proteins. The differences in cell surface protein composition between alveolar macrophages of smokers and nonsmokers may reflect their functional capabilities or their state of “activation” and may be mechanistically important in the development of various pulmonary diseases seen in smokers including cancer. These results also demonstrate that major changes in the surface proteins of the human alveolar macrophage plasma membrane can occur rapidly following manipulation.
Footnotes
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↵1 Supported in part by NIH Grants RO1-CA-36248 and RO1-HL-01308, Minnesota Medical Foundation Grant CRF-63-83, the Leukemia Task Force, and the Masonic Memorial Hospital Fund, Inc. Dr. Skubitz was a Fellow of the Leukemia Society of America. Dr. Northfelt was supported by a Zagaria Fellowship in Oncology from The Minnesota Medical Foundation. Dr. Hoidal was supported by an NIH Research Career Development Award (KO4-HL-32329). Presented in part at the annual meetings of The Central Society for Clinical Research, November 6–8, 1985, and the American Association for Cancer Research in Los Angeles, May 7–10, 1986; appears in abstract form in Clin. Res., 33: 383A, 1985, and Proc. Am. Assoc. Cancer Res., 27: 349, 1986.
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↵2 To whom requests for reprints should be addressed.
- Received October 21, 1986.
- Revision received February 16, 1987.
- Accepted March 20, 1987.
- ©1987 American Association for Cancer Research.