Biophysical regulation of Chlamydia pneumoniae-infected monocyte recruitment to atherosclerotic foci

摘要: Chlamydia pneumoniae infection is implicated in atherosclerosis although the contributory mechanisms are poorly understood. We hypothesize that C. favors recruitment of monocytes to atherosclerotic foci by altering monocyte biophysics. Primary, fresh human were infected with for 8 h, and interactions between E-selectin or aortic endothelium under flow characterized video microscopy image analysis. The distribution membrane lipid rafts adhesion receptors analyzed imaging cytometry. Infected cells rolled on endothelial surfaces, this rolling was slower, steady uniform compared uninfected cells. Infection decreases cholesterol levels, increases fluidity, disrupts rafts, redistributes CD44, which primary mediator interactions. Together, these changes translate higher firm endothelium, enhanced presence LDL. Uninfected treated LDL left untreated used as baseline control. Our results demonstrate biophysical due hyperlipidemia one key can exacerbate pathology. These findings provide a framework characterize role 'infectious burden' development progression atherosclerosis.