ABSTRACT
Effects of environmental (cold) stress and aging on cells in monocyte/macrophage lineage were investigated. We demonstrated that immune suppressive states seen in acute cold-stressed mice (8-10 weeks of age) is attributable to FcγRII(bright) suppressor macrophages. Serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of glucocorticoids (GC) receptor mRNA was observed in FcγRII(bright) cells from these mice. The increase of FcγRII(bright) cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of FcγRII(bright) cells in peritoneal exudate cells of control mice. These results suggest that the generation of FcγRII(bright) suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated by action of GC through the GC receptor. We likewise found that the proportion of FcγRII(bright) suppressor macrophages is increased in aged mice (22-24 months of age). Meanwhile, activated macrophages which function as antigen presenting cells were decreased in aged rats. Both the basal corticosterone concentrations in serum and the expression of mRNA for GC receptor in peritoneal macrophages increased significantly in aged animals, suggesting that these populational and functional changes of macrophages in aged animals were mediated, in part, by the increased basal levels of GC. This is probably being responsible for immunosenescence.
ABSTRACT
Effects of environmental (cold) stress and aging on cells in monocyte/macrophage lineage were investigated. We demonstrated that immune suppressive states seen in acute cold-stressed mice (8-10 weeks of age) is attributable to FcγRIIbright suppressor macrophages. Serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of glucocorticoids (GC) receptor mRNA was observed in FcγRIIbright cells from these mice. The increase of FcγRIIbright cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of FcγRIIbright cells in peritoneal exudate cells of control mice. These results suggest that the generation of FcγRIIbright suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated by action of GC through the GC receptor. We likewise found that the proportion of FcγRIIbright suppressor macrophages is increased in aged mice (22-24 months of age). Meanwhile, activated macrophages which function as antigen presenting cells were decreased in aged rats. Both the basal corticosterone concentrations in serum and the expression of mRNA for GC receptor in peritoneal macrophages increased significantly in aged animals, suggesting that these populational and functional changes of macrophages in aged animals were mediated, in part, by the increased basal levels of GC. This is probably being responsible for immunosenescence.
Subject(s)
Neisseria gonorrhoeae , Mice , MacrophagesABSTRACT
From the viewpoint of atherosclerosis prevention, it is important to examine the effects of exercise on the lipoprotein fraction in the postprandial state. The purpose of this study was to investigate the effects of a single period of low-intensity exercise on serum lipoprotein triacylglycerol (TG) after an oral fat load (50g/body surface area) as exogenous TG. Seven normolipidemic men aged 23.1±1.1 years (mean ± SEM) took part in two trials. The subjects were all young students at a university graduate school. In the exercise trial (Ex), they exercised for 1.5 h on a bicycle ergometer at 35-40% of their maximal oxygen uptake, starting 2 h after ingestion of the fat, and then rested for a further 2 h. In the control trial (Co), they rested for 5.5 h after ingestion of the fat. Lipoprotein and lipid levels were measured in venous blood taken during the fasted state and at different intervals between the two trials for 5.5 h after the fat load. Serum total TG and high-density lipoprotein (HDL) TG decreased significantly in Ex from 3.5 to 5.5h (p<0.05, p<0.01) in comparison with Co. These results indicate that a single period of low-intensity exercise reduces exogenous serum total TG and HDL-TG.
ABSTRACT
To study the effects of prolonged kendo practice in a hot environment on cardiovascular function, certain hemodynamic parameters were measured in 5 male college kendo fencers before and after 1 hour of kendo practice performed at a dry bulb temperature of 30.4t and wet bulb temperature of 26.2°C After kendo practice, body weight was significantly decreased and both hematocrit and blood viscosity were significantly increased. The left ventricular end-diastolic dimension and the left atrial dimension, measured by echocardiography, were significantly reduced after kendo practice, and stroke volume, ejection fraction, and fractional shortening were also significantly decreased after practice. The same fencers were subjected to lower body negative pressure testing designed to reduce the left ventricular end-diastolic dimension to the same degree as kendo practice, and comparable decreases in stroke volume, ejection fraction, and fractional shortening were observed. The ratio of end-systolic wall stress to end-systolic volume index was significantly increased during both kendo practice and lower body negative pressure testing. We conclude that prolonged kendo practice in a hot environment impairs cardiac pump function by reducing preload in parallel with the decrease in venous return, that myocardial contractility may not deteriorate despite marked hemoconcentration, and that fluid intake during practice may prevent deterioration of cardiovascular function.