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/cm2 enhanced the expression of pro‐inflammatory cytokine IL‐1β only in infected, but not in uninfected, monocytes. We also found that this enhancement is due to the upregulation of IL‐1β gene expression due to shear stress. Our results demonstrate that mechanotransduction is an important, heretofore unaddressed, determinant of inflammatory response to an infection. Biotechnol. Bioeng. 2015;112: 838–842. © 2014 Wiley Periodicals, Inc. Shear stress exacerbates the secretion of pro‐inflammatory cytokine IL‐1beta from Chlamydia pneumoniae‐infected but not from uninfected monocytes. The authors' results suggest that biophysical factors may play an important role in inflammatory response to infection.