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Growth Hormone Inhibits Apoptosis and Up-Regulates Reactive Oxygen Intermediates Production by Human Polymorphonuclear Neutrophils

Department of Surgery, University of Tokyo, Japan

Hideaki Saito, MD

Surgical Center, University of Tokyo, Japan

Tomomi Inoue, MD

Department of Surgery, University of Tokyo, Japan

Kazuhiko Fukatsu, MD

Department of Surgery, University of Tokyo, Japan

Ilsoo Han, MD

Department of Surgery, University of Tokyo, Japan

Satoshi Furukawa, MD

Department of Surgery, University of Tokyo, Japan

Shigeo Ikeda, MD

Department of Surgery, University of Tokyo, Japan

Tetsuichiro Muto, MD

Department of Surgery, University of Tokyo, Japan

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)

Journal of Parenteral and Enteral Nutrition, Vol. 22, No. 6, 368-374 (1998)
DOI: 10.1177/0148607198022006368


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