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(Journal of Leukocyte Biology. 2001;69:158-160.)
© 2001 by Society for Leukocyte Biology

Protein kinase C agonists enhance phagocytosis of P. aeruginosa by murine alveolar macrophages

John-Paul Heale and David P. Speert

Division of Infectious and Immunological Diseases, Department of Pediatrics, University of British Columbia, Vancouver, Canada

Correspondence: John-Paul Heale, University of British Columbia, Department of Pediatrics, Faculty of Medicine, The Research Institute, Room 381, 950 West 28th Avenue, Vancouver, BC, Canada, V5Z 4H4. E-mail: jpheale{at}interchange.ubc.ca

Pulmonary alveolar macrophages (AM{phi}s) are incompetent to phagocytose unopsonized Pseudomonas aeruginosa, but ingestion by other macrophage phenotypes (i.e., peritoneal macrophages) occurs efficiently. The purpose of this study was to explore factors that might control such phenotypic differences. Our laboratory has demonstrated that AM{phi}s exposed to sodium azide display enhanced phagocytosis of P. aeruginosa. Here we report that the phagocytic-enhancing effect of sodium azide was abrogated by inhibitors of protein kinase C (PKC). Furthermore, the addition of PKC agonists, such as phorbol myristate acetate (PMA), and tumor necrosis factor {alpha} (TNF-{alpha}), mimicked the phagocytic enhancing effect of sodium azide. We conclude that AM{phi}s are normally incompetent to phagocytose P. aeruginosa. Factors that up-regulate AM{phi} function (azide, PMA, TNF-{alpha}) can reverse the phagocytic incompetence in vitro. Although these compounds are not appropriate candidate therapeutic agents, their effects provide insights for understanding of the pathways responsible for regulation of P. aeruginosa phagocytosis.

Key Words: phorbol myristate acetate • tumor necrosis factor {alpha} • azide




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