Abstract
Toll-like receptors (TLRs) are dominant components of the innate immune system and have been targeted for therapeutic drug development for several inflammatory disorders including cancer, cardiovascular diseases, and diabetes mellitus. Daily levels of physical activity (PA) and dietary intake have been purported to influence the systemic circulation of cytokines, affecting the overall activation of TLRs and influencing the inflammatory milieu. The aim of this study is to investigate the association between daily physical activity and monocytic TLR2 expression in lean individuals. Normal-weight participants (n = 69) were recruited for this study. Daily physical activity was tracked for seven days using an ActiGraph accelerometer. The intensity of PA was determined by Freedson’s cut-offs, and participants were divided according to the 25th lowest (Q1), median (Q2), and top (Q3) percentiles of their activity level. Blood pressure measurements and heart rates were taken for each individual. Moreover, blood glucose, fasting insulin, cholesterol, high-density lipoprotein (HDL), and triglycerides were determined. Surface expression of TLR2 was quantified on peripheral monocytes by flow cytometry. Our data show that individuals with higher levels of moderate-to-vigorous PA and daily step count were found to have higher levels of circulatory CD14+TLR2+ subset. The top 25th percentile groups also showed significantly lower diastolic blood pressure (DBP), triglyceride (TG), and matrix metallopeptidase 9 (MMP9) levels in their circulation. Pearson correlation analysis revealed a negative relationship between CD14+TLR2+ subset and cardiovascular risk markers. The presented results highlight a positive influence of higher daily PA on cardiovascular health, driven by the upregulation of monocytic TLR2+ subsets in circulation, suggesting that TLR2 may play a modulatory role in the regulation of inflammation and lipid metabolism. Disclosure F. Bahman: None. H. Alsaeed: None. S. Albeloushi: None. F. Almulla: None. R. Ahmad: None. F. Alrashed: None.
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