ArticleBiotechnology and bioengineering2015
Shear stress upregulates IL-1β secretion by Chlamydia pneumoniae- infected monocytes.
Article in Biotechnology and bioengineering, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Mechanical cues orchestrate monocyte behavior in immune regulation and disease.APL bioengineering · 2025Review
- Biophysical regulation of Chlamydia pneumoniae-infected monocyte recruitment to atherosclerotic foci.Scientific reports · 2016Article
- Biophysical and Biochemical Outcomes of Chlamydia pneumoniae Infection Promotes Pro-atherogenic Matrix Microenvironment.Frontiers in microbiology · 2016Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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 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.
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