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On-Chip Endothelial Inflammatory Phenotyping
Published on: July 21, 2012
Interactions between stainless steel, shear stress, and monocytes
Regina L W Messer1, John Mickalonis, Jill B Lewis
1Department of Oral Biology and Maxillofacial Pathology, Medical College of Georgia, Augusta, Georgia, USA. rmesser@mail.mcg.edu
Journal of Biomedical Materials Research. Part A
|December 20, 2007
Summary
Monocytes interacting with stainless steel stents may alter stent corrosion and contribute to restenosis. This study found that monocytic cells activated by 316L stainless steel stents increased inflammatory cytokine secretion, a hallmark of in-stent restenosis.
Area of Science:
- Biomaterials Science
- Cardiovascular Research
- Immunology
Background:
- Coronary atherosclerosis is commonly treated with angioplasty and stainless steel stents.
- A significant percentage of these stents undergo restenosis within six months, driven by inflammation, monocyte infiltration, and cytokine release.
- The interplay between blood flow, monocytes, and stent corrosion in restenosis remains incompletely understood.
Purpose of the Study:
- To investigate the hypothesis that blood flow and monocytes interact to modify stent corrosion.
- To assess the impact of THP1 monocytes on the corrosion rate of 316L stainless steel (316LSS) under varying shear stress conditions.
- To determine the cytokine secretion profile of THP1 cells when exposed to 316LSS under simulated physiological flow.
Main Methods:
- Assessed 316LSS corrosion rates in the presence of THP1 monocytes under shear stress (0.5-50 dyn/cm²).
- Utilized cytokine arrays and ELISA to quantify THP1 cytokine secretion.
- Employed ANOVA and Tukey post hoc analysis for statistical comparison of data (alpha = 0.05).
Main Results:
- Monocytes significantly reduced 316LSS corrosion rates without affecting current density.
- Shear stress alone did not alter 316LSS corrosion rates, but THP1 cells adhered to the stent surface across all flow rates.
- Exposure to 316LSS and corrosion conditions under high flow increased secretion of seven cytokines, including IL8, involved in wound healing and inflammation.
- Elevated IL8 levels were comparable to a positive control, suggesting monocytic activation.
Conclusions:
- Monocytic cells may become activated upon exposure to 316LSS stents.
- This activation, evidenced by increased secretion of specific cytokines like IL8, could contribute to the development of in-stent restenosis.
- Altered stent corrosion in the presence of monocytes may be a factor in the restenosis process.
