Physical exercise is important for proper cardiovascular function and disease prevention, but it may influence the immune system. We evaluated the effect of strenuous exercise on monocyte chemotaxis. Monocytes were isolated from blood of 13 young, healthy, sedentary individuals participating in a three-week training program which consisted of repeated exercise bouts. Monocyte chemotaxis and serological biomarkers were investigated at baseline, after three weeks training and after four weeks recovery. Chemotaxis towards vascular endothelial growth factor-A (VEGF-A) and transforming growth factor-β1 (TGF-β1) was completely inhibited immediately after training (p<0.01), and remained so after four weeks recovery. Likewise, monocyte chemoattractant protein-1 (MCP-1)-induced migration declined after training (p<0.01) and improved only partially during the recovery period. MCP-1 serum levels were significantly reduced after four weeks recovery compared to baseline (p<0.01). Total blood antioxidant capacity was enhanced at this time point (p<0.01). Monocyte chemokinesis, TGF-β1 and nitric oxide serum levels remained unchanged during the study. Strenuous three-week training consisting of repeated exercise bouts in healthy, sedentary individuals reduces monocyte chemotaxis. It remains to be established, whether this is a sound adaptation to increased stimuli or an untoward reaction to overtraining. Nevertheless, the effect remains for several weeks with no exercise.
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Viruses
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Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA.
Monocytes are crucial players in innate immunity. The human cytomegalovirus (CMV) infection has significant impacts on monocyte effector functions and gene expression. CMV, a β-herpesvirus, disrupts key monocyte roles, including phagocytosis, antigen presentation, cytokine production, and migration, impairing their ability to combat pathogens and activate adaptive immune responses.
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January 2025
Department of Nutrition and Dietetics, Faculty of Health Sciences, Gazi University, Ankara 06490, Türkiye.
Endogenous and exogenous factors play a role in endothelial dysfunction. Inflammation, leukocyte adhesion-aggregation, abnormal vascular proliferation, atherosclerosis, and hypertension are among the endogenous factors. Another factor that affects endothelial dysfunction is exogenous factors such as drug treatments, smoking, alcohol, and nutrition.
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December 2024
Department of Ophthalmology, Zhongshan City People's Hospital, Zhongshan, Guangdong, China.
Background: Age-related macular degeneration (AMD), is a neurodegenerative ocular disease. This study investigated the role of ferroptosis-related genes and their interaction with immune cell infiltration in AMD.
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Cell and Molecular Tissue Engineering LLC, 14 Highwood Drive, Avon, 06001, CT, USA.
Continuous glucose monitoring (CGM) using implantable glucose sensors is a critical tool in the management of diabetes. Unfortunately, current commercial glucose sensors have limited performance and lifespans , considered to be due to sensor-induced tissue reactions (inflammation, fibrosis, and vessel regression). Previously, our laboratory utilized monocyte/macrophage (Mo/MQ) deficient and depleted mice to establish a causal relationship between Mo/MQ accumulation and inflammation in glucose sensor performance .
View Article and Find Full Text PDFCytotherapy
November 2024
Department of Otolaryngology-Head and Neck Surgery, Emory University School of Medicine, Atlanta, Georgia, USA; Department of Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia, USA; Department of Otolaryngology, Children's Healthcare of Atlanta, Atlanta, Georgia, USA. Electronic address:
Background Aims: Oral wound healing involves hemostasis, inflammation, proliferation and tissue remodeling. The oral cavity is a complex wound healing environment because of the presence of saliva, a high bacterial burden and ongoing physical trauma from eating. The inflammatory component of wound healing balances the polarization of macrophages in healing tissues between M1 inflammatory macrophages and M2 anti-inflammatory macrophages.
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