DIAGN MICROBIOL INFECT DIS 233 1985;3:233-242 Opsonic Activity of MCP-1 and MCP-2, Cationic Peptides from Rabbit Alveolar Macrophages Jacob Fleischmann, Michael E. Selsted, and Robert I. Lehrer MCP-1 and MCP-2, cationic peptides derived from rabbit alveolar macrophages, enhanced the ability of these ceils to ingest Staphylococcus aureus, Klebsiella pneumoniae, Bordetella bron- chiseptica r and Candida albicans in vitro. The opsonic effect of MCP-1 was potentiated by Ca +÷ and Mg+ + and was associated with binding of the peptide to alveolar macrophages and microorganisms. MCP-1 and MCP-2 may contribute to the ability of alveolar macrophage to ingest microorganisms that gain entry to the lower respiratory tract. INTRODUCTION Alveolar macrophage5 (AM), the first phagocytes likely to engage microorganisms that enter the lungs (Green and Kass, 1964; Green et al., 1977), may function in an environment that contains limited concentrations of the opsonic constituents of serum (Reynolds and Newball, 1974). We have previously reported that AM contain sub- stantial amounts of two cationic peptides MCP-1 and MCP-2, and suggested that these peptides may equip AM for various host-defense functions (Lehrer et al., 1983; Patterson-Delafield et al., 1980; Selsted et al., 1983). We now report that MCP-1 and MCP-2 possess opsonic activity for selected bacteria and fungi. MATERIALS AND METHODS Peptides MCP-1 and MCP-2 were purified to homogeneity from AM recovered from rabbits injected with complete Freund's adjuvant as previously described (Selsted et al., 1983). MCP-1 (1 mg) was iodinated by being exposed to 750 p, Ci of Na12SI, specific activity 17.4 mCi/mg (New England Nuclear, Boston, MA), for 80 min in 1 ml of 0.25 M sodium phosphate buffer, pH 7.0, in the presence of an Iodobead (Pierce Chemicals, Rockford, IL). Subsequently, 0.1 ml of KI solution (10 mg/ml) was added and 2 hr later the Iodobead was removed and the iodinated peptide was dialyzed exhaustively against 1% acetic acid at 4°C for 48 hr in Spectrapor 3 dialysis tubing. This is publication No. 37 of the Collaborative California Universities Mycology Research Unit (CCU-MRU). From the Divisions of Infectious Diseases (J.F.) and Hematology/Oncology (M.E.S.), Department of Medicine, UCLA School of Medicine, Los Angeles, C_,alifomia and Division of Hematology/Oncology, Department of Medicine, UCLA School of Medicine and VA Medical Center, West Los Angeles, California (R.I.L.). Address reprints to: Robert I. Lehrer, M.D., Professor of Medicine, Division of Hematol- ogy/Oncology, Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90024. Received May 21, 1984; revised and accepted September 5, 1984. © 1985 Elsevier Science Publishing Co., Inc. 52 Vanderbilt Avenue, New York, NY 10017 0732-8893/85/$03.30