title: Overload training inhibits phagocytosis and ROS generation of peritoneal macrophages: role of IGF-1 and MGF.
abstract: We tested the hypothesis that overload training inhibits the phagocytosis and the reactive oxygen species (ROS) generation of peritoneal macrophages (Mϕs), and that insulin-like growth factor-1(IGF-1) and mechano-growth factor (MGF) produced by macrophages may contribute to this process. Rats were randomized to two groups, sedentary control group (n = 10) and overload training group (n = 10). The rats of overload training group were subjected to 11 weeks of experimental training protocol. Blood sample was used to determine the content of hemoglobin, testosterone, and corticosterone. The phagocytosis and the ROS generation of Mϕs were measured by the uptake of neutral red and the flow cytometry, respectively. IGF-1 and MGF mRNA levels in Mϕs were determined by real-time PCR. In addition, we evaluated the effects of IGF-1 and MGF peptide on phagocytosis and ROS generation of Mϕs in vitro. The data showed that overload training significantly decreased the body weight (19.3 %, P < 0.01), the hemoglobin (13.5 %, P < 0.01), the testosterone (55.3 %, P < 0.01) and the corticosterone (40.6 %, P < 0.01) in blood. Moreover, overload training significantly decreased the phagocytosis (27 %, P < 0.05) and the ROS generation (35 %, P < 0.01) of Mϕs. IGF-1 and MGF mRNA levels in Mϕs from overload training group increased significantly compared with the control group (21-fold and 92-fold, respectively; P < 0.01). In vitro experiments showed that IGF-1 had no significant effect on the phagocytosis and the ROS generation of Mϕs. Unlike IGF-1, MGF peptide impaired the phagocytosis of Mϕs in dose-independent manner. In addition, MGF peptide of some concentrations (i.e., 1, 10, 50, 100 ng/ml) significantly inhibited the ROS generation of Mϕs. These results suggest that overload training inhibits the phagocytosis and the ROS generation of peritoneal macrophages, and that MGF produced by macrophages may play a key role in this process. This may represent a novel mechanism of immune suppression induced by overload training.
authors.affiliation: Department of Sports Medicine, Shanghai University of Sport, Shanghai 200438, China.
authors.forename: Weihua
authors.initials: W
authors.lastname: Xiao
authors.forename: Peijie
authors.initials: P
authors.lastname: Chen
authors.forename: Ru
authors.initials: R
authors.lastname: Wang
authors.forename: Jingmei
authors.initials: J
authors.lastname: Dong
mesh_terms: D000818:Animals; D007334:Insulin-Like Growth Factor I / Q000276:immunology*; D008264:Macrophages / Q000276:immunology*; D008297:Male; D010537:Peritoneum / Q000276:immunology / Q000473:pathology; D010587:Phagocytosis / Q000276:immunology*; D010805:Physical Conditioning, Animal / Q000379:methods*; D010807:Physical Endurance / Q000276:immunology*; D005082:Physical Exertion / Q000276:immunology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000276:immunology*; D050799:STAT5 Transcription Factor / Q000276:immunology*; D025521:Tumor Suppressor Proteins / Q000276:immunology*
chemical_list: D017382:Reactive Oxygen Species; D050799:STAT5 Transcription Factor; C494092:STAT5A protein, human; D025521:Tumor Suppressor Proteins; D007334:Insulin-Like Growth Factor I