Influence of Carbohydrate Ingestion on Cytokine Responses Following Acute Resistance Exercise

2003 ◽  
Vol 13 (4) ◽  
pp. 454-465 ◽  
Author(s):  
Marcia A. Chan ◽  
Alexander J. Koch ◽  
Stephen H. Benedict ◽  
Jeffrey A. Potteiger

The effect of carbohydrate supplementation (CHO) on interleukin 2 (IL-2) and interleukin 5 (IL-5) secretion following acute resistance exercise was examined in 9 resistance-trained males. Subjects completed a randomized, double-blind protocol with exercise separated by 14 days. The exercise consisted of a high intensity, short rest interval squat workout. Subjects consumed 1.0 g · kg body mass-1 CHO or an equal volume of placebo (PLC) 10 min prior to and 10 min following exercise. Blood was collected at rest (REST), immediately post exercise (POST), and at 1.5 h of recovery (1.5 h POST). Isolated peripheral blood mononuclear cells were stimulated with PHA and assayed for IL-2 and IL-5 secretion. IL-2 secretion was significantly decreased at POST for both the PLC and CHO groups. However, the degree of decrease was less in the CHO group (16%) than in the PLC group (48%), and this difference was statistically significant. These responses were transient, and the values returned to normal by 1.5 h POST. A mild and transient but significant decrease in IL-5 secretion by the PLC group was observed at POST (26%) compared to REST. No significant decrease was observed in IL-5 secretion for CHO from REST to POST (12%). These data support a possible effect of carbohydrate supplementation on IL-2 and IL-5 secretion following high-intensity resistance exercise.

2001 ◽  
Vol 11 (2) ◽  
pp. 149-161 ◽  
Author(s):  
Alexander J. Koch ◽  
Jeffrey A. Potteiger ◽  
Marcia A. Chan ◽  
Stephen H. Benedict ◽  
Bruce B. Frey

The effect of carbohydrate supplementation (CHO) on the lymphocyte response to acute resistance exercise was examined in 10 resistance-trained males. Subjects completed a randomized double-blind protocol with sessions separated by 14 days. The exercise session consisted of a high intensity, short rest interval squat workout. Subjects consumed 1.0 g · kg body mass−1 CHO or an equal volume of placebo (PLC) 10 min prior to and 10 min following exercise. Blood was collected at rest (REST), immediately post exercise (POST), and at 1.5 hours and 4.0 hours of recovery, and analyzed for plasma glucose, serum cortisol, leukocyte subsets, and phytohemagglutinin (PHA)-stimulated lymphocyte proliferation. A significant Treatment × Time effect was observed for lymphocyte proliferation between CHO and PLC, but post hoc analyses revealed no between-treatment differences at any post-exercise time point. Lymphocyte proliferation was significantly depressed below REST at POST (−39.2% for PLC, −25.7% for CHO). Significant fluctuations in leukocyte subset trafficking were observed for both treatments at POST, 1.5 hours, and 4.0 hours. Plasma glucose was significantly increased POST in CHO compared to PLC. Cortisol was significantly increased from REST to POST in both treatments. These data support a minimal effect of carbohydrate ingestion on the lymphocyte response to high-intensity resistance exercise.


2002 ◽  
Vol 12 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Nicolette C. Bishop ◽  
Michael Gleeson ◽  
Ceri W. Nicholas ◽  
Ajmol Ali

Ingesting carbohydrate (CHO) beverages during prolonged, continuous heavy exercise results in smaller changes in the plasma concentrations of several cytokines and attenuates a decline in neutrophil function. In contrast, ingesting CHO during prolonged intermittent exercise appears to have negligible influence on these responses, probably due to the overall moderate intensity of these intermittent exercise protocols. Therefore, we examined the effect of CHO ingestion on plasma interIeukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS)-stimuIated neutrophil degranulation responses to high-intensity intermittent running. Six trained male soccer players performed 2 exercise trials, 7 days apart, in a randomized, counterbalanced design. On each occasion, they completed six 15-min periods of intermittent running consisting of maximal sprinting interspersed with less intense periods of running and walking. Subjects consumed either CHO or artificially sweetened placebo(PLA) beverages immediately before and at 15-min intervals during the exercise. At 30 min post-exercise, CHO versus PLA was associated with a higher plasma glucose concentration (p< .01), a lower plasma cortisol and IL-6 concentration (p < .02), and fewer numbers of circulating neutrophils (p < .05). Following the exercise, LPS-stimulated elastase release per neutrophil fell 31 % below baseline values on the PLA trial (p = .06) compared with 11% on the CHO trial (p = .30). Plasma TNF-α concentration increased following the exercise (main effect of time, p < .001) but was not affected by CHO. These data indicate that CHO ingestion attenuates changes in plasma IL-6 concentration, neutrophil trafficking, and LPS-stimulated neutrophil degranulation in response to intermittent exercise that involves bouts of very high intensity exercise.


2021 ◽  
Vol 9 (1) ◽  
pp. e001762
Author(s):  
Punit Upadhyaya ◽  
Johanna Lahdenranta ◽  
Kristen Hurov ◽  
Sailaja Battula ◽  
Rachel Dods ◽  
...  

BackgroundIn contrast to immune checkpoint inhibitors, the use of antibodies as agonists of immune costimulatory receptors as cancer therapeutics has largely failed. We sought to address this problem using a new class of modular synthetic drugs, termed tumor-targeted immune cell agonists (TICAs), based on constrained bicyclic peptides (Bicycles).MethodsPhage libraries displaying Bicycles were panned for binders against tumor necrosis factor (TNF) superfamily receptors CD137 and OX40, and tumor antigens EphA2, Nectin-4 and programmed death ligand 1. The CD137 and OX40 Bicycles were chemically conjugated to tumor antigen Bicycles with different linkers and stoichiometric ratios of binders to obtain a library of low molecular weight TICAs (MW <8 kDa). The TICAs were evaluated in a suite of in vitro and in vivo assays to characterize their pharmacology and mechanism of action.ResultsLinking Bicycles against costimulatory receptors (e.g., CD137) to Bicycles against tumor antigens (e.g., EphA2) created potent agonists that activated the receptors selectively in the presence of tumor cells expressing these antigens. An EphA2/CD137 TICA (BCY12491) efficiently costimulated human peripheral blood mononuclear cells in vitro in the presence of EphA2 expressing tumor cell lines as measured by the increased secretion of interferon γ and interleukin-2. Treatment of C57/Bl6 mice transgenic for the human CD137 extracellular domain (huCD137) bearing EphA2-expressing MC38 tumors with BCY12491 resulted in the infiltration of CD8+ T cells, elimination of tumors and generation of immunological memory. BCY12491 was cleared quickly from the circulation (plasma t1/2 in mice of 1–2 hr), yet intermittent dosing proved effective.ConclusionTumor target-dependent CD137 agonism using a novel chemical approach (TICAs) afforded elimination of tumors with only intermittent dosing suggesting potential for a wide therapeutic index in humans. This work unlocks a new path to effective cancer immunotherapy via agonism of TNF superfamily receptors.


2021 ◽  
Vol 22 (15) ◽  
pp. 7988
Author(s):  
Andrea Coppola ◽  
Barbara Capuani ◽  
Francesca Pacifici ◽  
Donatella Pastore ◽  
Roberto Arriga ◽  
...  

Activation of innate immunity and low-grade inflammation contributes to hyperglycemia and an onset of Type 2 Diabetes Mellitus (T2DM). Interleukin-2 (IL-2), leptin, High Mobility Group Box-1 (HMGB-1), and increased glucose concentrations are mediators of these processes also by modulating peripheral blood mononuclear cells (PBMCs) response. The aim of this study was to investigate if HMGB-1 and IL-2 turn on PBMCs and their leptin secretion. In isolated human PBMCs and their subpopulations from healthy individuals and naïve T2DM patients, leptin release, pro-inflammatory response and Toll-like Receptors (TLRs) activation was measured. After treatment with IL-2 and HMGB1, NK (Natural Killer) have the highest amount of leptin secretion, whilst NK-T have the maximal release in basal conditions. TLR4 (TAK242) and/or TLR2 (TLR2-IgA) inhibitors decreased leptin secretion after IL-2 and HMGB1 treatment. A further non-significant increase in leptin secretion was reported in PBMCs of naive T2DM patients in response to IL-2 and HMGB-1 stimulation. Finally, hyperglycemia or hyperinsulinemia might stimulate leptin secretion from PBMCs. The amount of leptin released from PBMCs after the different treatments was enough to stimulate the secretion of IL-1β from monocytes. Targeting leptin sera levels and secretion from PBMCs could represent a new therapeutic strategy to counteract metabolic diseases such as T2DM.


1996 ◽  
Vol 271 (5) ◽  
pp. G841-G848 ◽  
Author(s):  
J. M. Klapproth ◽  
M. S. Donnenberg ◽  
J. M. Abraham ◽  
S. P. James

Previously we have shown that lysates of enteropathogenic Escherichia coli (EPEC) inhibit lymphokine production by mitogen-activated peripheral blood mononuclear cells (PBMCs). The aim of the present study was to determine whether products of EPEC alter lymphokine expression by gastrointestinal mucosal lymphocytes. Lysates from EPEC clones inhibited mitogen-stimulated interleukin-2 (IL-2), IL-4, IL-5, and interferon-gamma (IFN-gamma) but not IL-8 mRNA expression by lamina propria mononuclear cells isolated from surgically resected colon specimens. Inhibitory lysates did not significantly change CD25 expression on either CD4, CD8, or CD45R0 lymphocytes by flow cytometry. Bacterial supernatants of EPEC inhibited IL-2 and IL-5 protein secretion by mitogen-stimulated PBMCs. EPEC lysates inhibited IL-2 mRNA expression induced by lysates of nonpathogenic E. coli. In conclusion, EPEC contains a novel gene(s) that encodes factors that selectively inhibit IL-2, IL-4, IL-5, and IFN-gamma expression by mucosal mononuclear cells without affecting CD25 or IL-8 expression. Thus enteric bacteria can produce factors that may regulate the function of the gastrointestinal mucosal immune system.


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