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In vitro culture of murine peritoneal and alveolar macrophages modulates phagocytosis of Pseudomonas aeruginosa and glucose transport
Author(s) -
Everett Karin D. E.,
Barghouthi Sameer,
Speert David P.
Publication year - 1996
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.59.4.539
Subject(s) - phagocytosis , fructose , glut1 , glucose transporter , biology , pseudomonas aeruginosa , microbiology and biotechnology , mannose , macrophage , biochemistry , in vitro , bacteria , endocrinology , insulin , genetics
Phagocytosis by murine peritoneal macrophages (PMφ) 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 PMφ and to murine alveolar macrophages (AMφ). Fructose‐cultured PMφ developed fructose‐dependent phagocytosis of P. aeruginosa with increased glucose‐dependent phagocytosis, GLUT1 expression, and [ 14 C]glucose transport. Freshly explanted AMφ, which were unable to transport [ 41 C]ghicose 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 AMφ 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 AMφ phagocytic function and may therefore possibly improve pulmonary host defense against P. aeruginosa.