In vitro culture of murine peritoneal and alveolar macrophages modulates phagocytosis of Pseudomonas aeruginosa and glucose transport.

Phagocytosis by murine peritoneal macrophages (PM phi) of unopsonized Pseudomonas aeruginosa is a novel, glucose-dependent process occurring in concert with glucose or mannose transport via the GLUT1 facilitative transporter. The mechanism by which this transport triggers phagocytosis is not understood. The purpose of these investigations was to improve our understanding of this mechanism by delivery of an alternative sugar (fructose) to PM phi and to murine alveolar macrophages (AM phi). Fructose-cultured PM phi developed fructose-dependent phagocytosis of P. aeruginosa with increased glucose-dependent phagocytosis, GLUT1 expression, and [14C]glucose transport. Freshly explanted AM phi, which were unable to transport [14C]glucose or to ingest P. aeruginosa acquired the ability to transport glucose and to phagocytose P. aeruginosa with culture in either glucose or fructose. Both fructose- and glucose-cultured AM phi remained viable but incapable of measurable fructose transport or fructose-dependent phagocytosis. These studies suggest that an intracellular metabolite of fructose, glucose, and mannose is involved in triggering macrophage phagocytosis of P. aeruginosa. We demonstrate that delivery of appropriate substrates can substantially improve AM phi phagocytic function and may therefore possibly improve pulmonary host defense against P. aeruginosa.