title: Growth hormone and insulin-like growth factor I augment bactericidal capacity of human polymorphonuclear neutrophils.
abstract: Effects of growth hormone (GH) and insulin-like growth factor (IGF)-I on bactericidal capacity of human polymorphonuclear neutrophils (PMNs) were investigated. Venous blood was collected from healthy volunteers. In Experiment 1, PMNs were isolated, incubated with GH or IGF-I, and cocultured with Escherichia coli. E. coli-killing capacity, viability, and CD11b and CD16 expressions of PMNs were then assessed. Both GH and IGF-I enhanced E. coli killing by PMNs. GH preserved PMN viability during E. coli killing, whereas IGF-I enhanced PMN CD11b expression before coculture with E. coli. In Experiment 2, whole blood was washed and incubated with GH or IGF-I. PMNs in washed whole blood were then analyzed for phorbol myristate acetate (PMA)-stimulated CD11b, CD35, and CD16 expressions and production of reactive oxygen intermediates (ROI), as well as phagocytosis with/without anti-CD11b antibody. IGF-I enhanced PMN expressions of CD11b and CD35, but not CD16, stimulated with PMA. Both hormones enhanced phagocytosis, which was abrogated by anti-CD11b antibody, and intracellular ROI production by PMNs. These results indicate that both GH and IGF-I augment human PMN bactericidal capacity, via increased phagocytosis and intracellular ROI production. Preservation of PMN viability by GH and enhanced complement receptor expression by IGF-I may also be associated with augmented PMN bactericidal capacity. Although PMN activation has potentially harmful aspects, these results encourage additional studies to confirm the clinical relevance of exogenous GH or IGF-I for the prevention or management of septic complications in perioperative or critically ill patients especially with low circulating GH and/or IGF-I levels.
authors.affiliation: Department of Surgery I, University of Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
authors.forename: K
authors.initials: K
authors.lastname: Fukatsu
authors.forename: I
authors.initials: I
authors.lastname: Han
authors.forename: S
authors.initials: S
authors.lastname: Furukawa
authors.forename: S
authors.initials: S
authors.lastname: Ikeda
authors.forename: T
authors.initials: T
authors.lastname: Muto
mesh_terms: D002470:Cell Survival; D002478:Cells, Cultured; D018920:Coculture Techniques; D004305:Dose-Response Relationship, Drug; D004926:Escherichia coli; D019382:Human Growth Hormone / Q000494:pharmacology*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000494:pharmacology*; D016177:Macrophage-1 Antigen / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000382:microbiology* / Q000502:physiology*; D010587:Phagocytosis; D017382:Reactive Oxygen Species / Q000378:metabolism; D017463:Receptors, Complement 3b; D017452:Receptors, IgG / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D016177:Macrophage-1 Antigen; D017382:Reactive Oxygen Species; D017463:Receptors, Complement 3b; D017452:Receptors, IgG; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I; D013755:Tetradecanoylphorbol Acetate