Experiments including cell and animal models investigate the molecular mechanisms underlying the regulation of homeostasis and function of monocytes.

Diet-induced obesity in mice led to a duration of diet-dependent bone marrow adipocyte whitening, which drove monocyte expansion and skewing towards a tissue-invasive phenotype, likely contributing to ensuing tissue infiltration that accompanies obesity and diabetes.

By altering monocyte development, pristane exposure could generate activated Ly6C^hi and Ly6C^lo/− monocytes, contributing to lung microvascular endothelial injury and DAH susceptibility.