Shear stress upregulates IL-1β secretion by Chlamydia pneumoniae- infected monocytes.

ABSTRACT: Infectious agents are increasingly implicated in the development and progression of chronic inflammatory diseases. Several lines of evidence suggest that the common intracellular respiratory pathogen, Chlamydia pneumoniae contributes to the well-established risk factors of atherosclerosis but the exact mechanism is not well understood. It is believed that C. pneumoniae-infected monocytes travel from the lung to the atherosclerotic foci, during which the cells experience mechanical stimuli due to blood flow. In this work, we characterized the effect of physiological levels of shear stress on C. pneumoniae-infected human monocytes in an in vitro flow model. We found that a shear stress of 5 dyn/cm(2) enhanced the expression of pro-inflammatory cytokine IL-1β only in infected, but not in unin

SUBMITTER: Cheeniyil A 

PROVIDER: S-EPMC4427049 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature