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This article examines the effects of exercise on immune function, specifically inflammation and cardiovascular health. It discusses how exercise can stimulate the production of anti-inflammatory cytokines and leukocytes, aiding in tissue repair and reducing inflammation. However, intense exercise has been found to temporarily suppress the immune system and decrease the effectiveness of anti-inflammatory cytokines in individuals at risk for heart disease. The study also investigates the impact of exercise on monocyte polarization and finds that exercise does not significantly influence the polarization of monocytes towards pro-inflammatory or anti-inflammatory states. The study emphasizes the importance of measuring both anti-inflammatory activity and phenotype polarization when studying the effects of exercise on inflammation. Further research is needed to understand the effects of different exercise protocols on immune function, particularly in less active individuals, and to explore sex differences. Additionally, more research is warranted on the mechanisms by which exercise affects monocyte subset polarization and the production and effects of other inflammatory cytokines. Overall, this study provides valuable insights into the relationship between exercise and inflammation, laying the groundwork for future research in exercise immunology. [Extracted from the article]

Aims: Following ST-segment elevation myocardial infarction (STEMI), recruitment and activation of monocytes [classical (CD14++CD16-CCR2++), intermediate (CD14++CD16+CCR2+), non-classical (CD14LowCD16++CCR2Low)] are needed for myocardial wound healing. Monocyte surface receptor CC chemokine receptor type 2 (CCR2) is responsible for monocyte chemotaxis to sites of inflammation and the lipopolysaccharide (LPS)-binding protein co-receptor, CD14, is involved in pro-inflammatory monocyte activation. The purpose of this investigation was to determine the effects of ex-vivo LPS activation on monocyte subset CD14 and CCR2 expression in post-STEMI individuals with normal and elevated random blood glucose.Methods: Post-STEMI subjects were identified as normal random glucose (NG, <98 mg/dL, n = 13) or impaired random glucose (IG, ≥98 mg/dL, n = 26) and monocytes were analyzed for non-activated and LPS-activated (1 µg/mL for 4 h) CCR2 and CD14 expression.Results: Non-activated intermediate monocytes from IG showed decreased CD14 expression when compared to NG, which was maintained following LPS-activation. The NG group showed a larger absolute reduction in classical CCR2 expression, leading to a significant difference between NG and IG following LPS-activation.Conclusion: Results suggest a heightened response to pro-inflammatory activation in IG following STEMI, which may impair or delay post-STEMI myocardial healing, and thus increase the incidence of chronic heart failure. NIH 1R34HL121402. [ABSTRACT FROM AUTHOR]