A South Asian (SA) cardiovascular phenomenon exists whereby SAs have excess burden of cardiovascular disease (CVD) despite having low prevalence of recognized CVD risk factors. The aim of the current study was to determine whether perturbations in monocyte biology contribute to this phenomenon via higher circulating cell numbers, a more pro-inflammatory phenotype, and higher transmigration and adhesion. Adhesion is linked to vascular inflammation whereas transmigration is linked to tissue inflammation. SA men with (N = 10; SAs with central obesity [CO-SA]) and without (N = 10; lean SA [LE-SA]) central obesity, plus White European counterparts (N = 10; white Europeans with central obesity [CO-WE], N = 10; lean white Europeans [LE-WE]) participated. An ex vivo assay mimicking blood flow dynamics coupled to flow cytometry determined the adhesion and transmigration of monocyte subsets toward chemokine-rich media cultured from pre-adipocytes (absolute responses). Migration and adhesion were also standardized for differences in numbers of circulating monocytes between participants (relative responses). Metabolic and inflammatory markers were assessed. SAs had higher absolute (but not relative) adhesion and migration of monocytes than WEs. Central obesity was associated with higher absolute and relative adhesion and migration of monocytes. SAs had higher concentrations of all monocyte subsets compared with WEs coinciding with adverse cardiovascular-inflammatory profiles. LE-SAs had similar monocyte concentrations, transmigration, and adhesion compared with CO-WEs, corresponding with similar cardiovascular-inflammatory profiles. The study provides novel evidence for higher monocyte counts associated with higher transmigration and adhesion in SA compared with WE men. Importantly, similar monocyte biology and cardiovascular-inflammatory profiles were seen in LE-SAs compared with CO-WEs, which may contribute to the higher risk of CVD at lower body mass index experienced by SAs.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10681421PMC
http://dx.doi.org/10.14814/phy2.15883DOI Listing

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