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Growth Hormone Inhibits Apoptosis and Up‐Regulates Reactive Oxygen Intermediates Production by Human Polymorphonuclear Neutrophils
Author(s) -
Matsuda Takeaki,
Saito Hideaki,
Inoue Tomomi,
Fukatsu Kazuhiko,
Han Ilsoo,
Furukawa Satoshi,
Ikeda Shigeo,
Muto Tetsuichiro
Publication year - 1998
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607198022006368
Subject(s) - cd16 , apoptosis , monocyte , flow cytometry , reactive oxygen species , medicine , endocrinology , programmed cell death , phagocytosis , biology , immune system , microbiology and biotechnology , immunology , chemistry , cd3 , biochemistry , cd8
Background: Growth hormone (GH) regulates the immune and metabolic systems; however, the effects of GH on the functions and cell death of polymorphonuclear neutrophils (PMNs) are not well understood. Therefore, this study was designed to investigate the effects of GH on PMN apoptosis, reactive oxygen intermediates (ROI) production, CD16, and Fas expression. We also investigated the effects of GH on the functions of other circulating leukocytes (ie, monocytes and lymphocytes). Methods: Venous blood was collected from healthy volunteers. Whole blood was washed and pretreated with GH (0 or 100 ng/mL) for 3 hours and then cultured for 0, 4, or 12 hours. PMNs in washed whole blood were analyzed by flow cytometry for cell death, phorbol myristate acetate‐stimulated ROI production, CD16, and Fas expression at each time point. Morphologic features also were assessed. PMN apoptosis was confirmed by chromatin staining and DNA gel electrophoresis. Results: GH inhibited PMN apoptosis at 12 hours of culture. GH enhanced ROI production by PMNs and monocytes throughout the 12‐hour culture but had no effects on CD16 expression on PMNs. Furthermore, GH decreased Fas expression on PMNs at 4 hours of culture. However, there were no effects of GH on apoptosis of monocytes or lymphocytes for the duration of this experiment. Conclusions: GH pretreatment down‐regulates Fas expression on PMNs, inhibits apoptosis, and up‐regulates ROI production. GH pretreatment also increases monocyte ROI production. Although activated PMNs have potentially harmful aspects, our results suggest that GH may improve host defense, mainly through enhancement of the PMN functional life span. (Journal of Parenteral and Enteral Nutrition 22: 368–374, 1998)