Biomedical subjects

D A Henson

Publications and source records attributed to D A Henson.

40 records · Page 3Linked to original sources

PubMed1993

Effects of high- vs moderate-intensity exercise on natural killer cell activity.

The effect of 45 min of high- (80% VO2max) vs moderate- (50% VO2max) intensity treadmill exercise on natural killer cell cytotoxic activity (NKCA) was investigated in 10 well-conditioned (66.0 +/- 1.9 ml.kg-1.min-1), young males (22.1 +/- 1.3 yr). Blood samples were taken before and immediately after exercise, with three more samples taken during 3.5 h of recovery, and analyzed for proportion of NK cells (CD3-CD16+CD56+) and NKCA. Exercise at 80% vs 50% VO2max resulted in a greater immediate postexercise increase in proportion of NK cells, followed by a 1-h and 2-h decrease below preexercise levels for both intensity conditions. NKCA rose significantly above preexercise levels following high- but not moderate-intensity exercise. For both exercise intensity conditions, NKCA tended to drop below preexercise levels by 1 h postexercise, rising back to preexercise levels by 3.5 h postexercise. When NKCA was expressed on a per-NK cell basis, however, no change relative to preexercise levels occurred following moderate-intensity exercise, while a significant increase occurred after 2-h recovery from high-intensity exercise. These data demonstrate that both high- and moderate-intensity exercise are associated with significant shifts in circulating proportions of NK cells which significantly influence interpretation of NKCA data based on assays using separated mononuclear cells.

Adolescent↗

PubMed1992

Effects of brief, heavy exertion on circulating lymphocyte subpopulations and proliferative response.

Ten healthy males (mean age 22.3 +/- 0.8 yr) pedaled with maximal effort for 30 s against a workload adjusted prior to the start of the test to 0.98 N.kg body mass-1. Blood samples were collected before, and 3 min and 1 h following exercise. Peak and average power mean values were 1020 +/- 51 and 738 +/- 34 W, respectively. Total leukocytes increased 40% in response to the exercise bout, but were 16% below pretest levels after 1 h of recovery (F = 123, P < 0.001). Neutrophils and lymphocytes represented approximately 60% and 30% of the leukocytosis, respectively. Lymphocytes increased 30% following exercise, but were 36% below pretest levels after 1 h recovery (F = 56.4, P < 0.001). The post-test lymphocytosis can be explained primarily from the 176% increase in natural killer cells (NK) and 28% increase in cytotoxic/suppressor T cells, while the 1-h recovery lymphopenia occurred because of a sharp decrease in total T cells and a moderate decrease in NK cells. No significant changes in lymphocyte proliferative response or serum immunoglobulin levels were found when appropriate adjustments for changes in plasma volume or lymphocyte subset changes were made. Plasma epinephrine increased 300% in response to the exercise bout, and best explains the measured changes in circulating levels of lymphocyte subsets. These results demonstrate that changes in circulating levels of leukocyte and lymphocyte subsets, especially NK cells, occur rapidly in response to 30 s of brief, heavy exertion.

Adult↗

PubMed1989

Morphological characterization of beta-VLDL and acetylated-LDL binding and internalization by cultured pigeon monocytes.

The ultrastructure of binding, internalization, and translocation of beta-migrating very low density lipoprotein (beta-VLDL) and acetylated low density lipoprotein (Ac-LDL) by cultured pigeon monocytes was examined using lipoprotein-gold conjugates. Through morphometry, differences in the binding and uptake of beta-VLDL-gold and Ac-LDL-gold were documented. Cells exposed to either beta-VLDL-gold or Ac-LDL-gold for 2 hr at 4 degrees C had the label over noncoated regions of the plasma membrane. Upon warming the cells to 37 degrees C for 2 min, 35% of the surface-bound beta-VLDL-gold was within coated pits on the cell surface. Although coated pits occupied less than 2% of the surface, binding of beta-VLDL-gold was 53 times more concentrated in coated pits as compared to noncoated membrane regions. In contrast, Ac-LDL-gold neither bound to coated pits nor relocated into coated regions of the membrane upon warming to 37 degrees C. Both the beta-VLDL-gold and the Ac-LDL-gold were internalized when the cells were rewarmed at 37 degrees C. Most of the internalized gold particles for both lipoproteins were located in electron-lucent vesicles; however, 9% of the intracellular beta-VLDL-gold was observed within coated vesicles at early times. Upon prolonged rewarming (30-90 min), both lipoprotein-gold conjugates were within acid phosphatase-positive lysosomes. Ultimately 83% of the Ac-LDL-gold and 90% of the beta-VLDL-gold were within electron-dense and electron-lucent lysosomes. These results suggested that the receptor-mediated binding and internalization of beta-VLDL and Ac-LDL by pigeon monocyte macrophages proceeded by separate, distinct routes; beta-VLDL by both coated and noncoated pathways while Ac-LDL was internalized exclusively by noncoated mechanisms. Regardless of these internalization differences, both lipoproteins were delivered to lysosomes for degradation.

Acid Phosphatase↗

PubMed1989

beta-VLDL and acetylated-LDL binding to pigeon monocyte macrophages.

Blood-derived monocytes are an important source of foam cells in atherosclerotic lesions of White Carneau pigeons. Based upon studies with cultured blood monocytes (monocyte macrophages) and peritoneal macrophages from a variety of mammalian species, it has been proposed that these cells become loaded with cholesteryl esters through the uptake of lipoproteins including beta-migrating very low density lipoproteins (beta-VLDL) and low density lipoproteins that have been chemically modified in a manner analogous to experimental acetylation (Ac-LDL). The purpose of this study was to determine whether similar mechanisms functioned in pigeon monocyte macrophages. Radioiodinated pigeon beta-VLDL and Ac-LDL were incubated with White Carneau pigeon monocyte macrophages that had been maintained in culture for 7 days. Scatchard analysis of the specific binding data revealed the presence of specific and saturable receptors for both beta-VLDL and Ac-LDL. beta-VLDL receptors had both low and high affinity binding components, whereas Ac-LDL receptors displayed a single class of high affinity binding sites. beta-VLDL binding remained relatively constant from 3 to 10 days in culture while Ac-LDL binding increased with time in culture. Competition studies demonstrated a high degree of binding specificity for 125I-Ac-LDL, but less for 125I-beta-VLDL. Binding of 125I-beta-VLDL was not competed for by Ac-LDL, but was by beta-VLDL and by low density lipoproteins from both normal and hypercholesterolemic pigeons. Following binding of beta-VLDL and Ac-LDL, the lipoproteins were rapidly internalized and degraded. Although the majority of degradation was secondary to internalization by the monocyte macrophages, approx. 5% of the degradation resulted from enzymatic activity in the culture medium, presumably due to secretion of proteolytic enzymes by the cells. As measured by esterification of [14C]oleate to cholesterol, it was shown that the cholesterol liberated from the degradation of both beta-VLDL and Ac-LDL stimulated cholesteryl ester synthesis in pigeon monocyte macrophages. These studies confirm the existence of specific beta-VLDL and Ac-LDL receptors on the surface of pigeon monocyte macrophages which facilitate both internalization of the lipoproteins and subsequent stimulation of cholesteryl ester synthesis. This is the first demonstration of beta-VLDL and Ac-LDL receptors on monocyte macrophages from an avian species, and the findings support the potential role for the receptor-mediated uptake of a variety of abnormal lipoproteins in the formation of monocyte-derived foam cells in the arterial wall of White Carneau pigeons during the development of atherosclerosis.

Animals↗