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Published on: May 8, 2016
Endothelial microparticles (EMP) bind and activate monocytes: elevated EMP-monocyte conjugates in multiple sclerosis
Wenche Jy1, Alireza Minagar, Joaquin J Jimenez
1The Wallace H. Coulter Platelet Laboratory, Department of Medicine, University of Miami School of Medicine, Miami, FL 33136, USA. wjy@med.miami.edu
Abstract:
Elevated plasma endothelial microparticles (EMP) have been documented in MS during exacerbation. However, the role of EMP in pathogenesis of MS remains unclear. We investigated the formation of EMP-monocyte conjugates (EMP-MoC) and their potential role in transendothelial migration of inflammatory cells in MS. EMP-MoC were assayed in 30 MS patients in exacerbation, 20 in remission and in 35 controls. EMP-leukocyte conjugation was investigated flowcytometrically by employing alpha-CD54 or alpha-CD62E for EMP, and alpha-CD45 for leukocytes. EMP-MoC were characterized by identifying adhesion molecules involved and their effect on monocyte function. In vivo (clinical): EMP-MoC were markedly elevated in exacerbation vs. remission and controls, correlating with presence of GD+ MRI lesions. Free CD54+ EMP were not elevated but free CD62E+ EMP were. In vitro: EMP bound preferentially to monocytes, less to neutrophils, but little to lymphocytes. Bound EMP activated monocytes: CD11b expression increased 50% and migration through cerebral endothelial cell layer increased 2.6-fold. Blockade of CD54 reduced binding by 80%. Most CD54+ EMP bound to monocytes, leaving little free EMP, while CD62+ EMP were found both free and bound. These results demonstrated that phenotypic subsets of EMP interacted differently with monocytes. Based on our observations, EMP may enhance inflammation and increase transendothelial migration of monocytes in MS by binding to and activating monocytes through CD54. EMP-MoC were markedly increased in MS patients in exacerbation compared to remission and may serve as a sensitive marker of MS disease activity.
Insights
Endothelial microparticles (EMP) form conjugates with monocytes, increasing inflammation and cell migration in multiple sclerosis (MS) during exacerbation. These EMP-monocyte conjugates (EMP-MoC) may serve as a key marker for MS disease activity.
Area of Science:
- Neuroimmunology
- Vascular Biology
- Cellular Biology
Background:
- Elevated plasma endothelial microparticles (EMP) are observed in multiple sclerosis (MS) during exacerbation.
- The precise role of EMP in MS pathogenesis, particularly in inflammatory cell trafficking, remains incompletely understood.
Purpose of the Study:
- To investigate the formation of EMP-monocyte conjugates (EMP-MoC) in MS.
- To determine the role of EMP-MoC in the transendothelial migration of inflammatory cells in MS.
- To assess EMP-MoC as a potential biomarker for MS disease activity.
Main Methods:
- Flow cytometry was used to quantify EMP-leukocyte conjugation, specifically EMP-monocyte conjugates (EMP-MoC), in MS patients during exacerbation and remission, and in controls.
- Adhesion molecules involved in EMP-MoC formation were identified using antibodies against CD54 and CD62E for EMP, and CD45 for leukocytes.
- In vitro assays assessed the effect of bound EMP on monocyte activation (CD11b expression) and their migratory capacity across a cerebral endothelial cell layer.
Main Results:
- EMP-MoC levels were significantly elevated in MS patients during exacerbation compared to remission and controls, correlating with Gadolinium-enhancing (GD+) MRI lesions.
- In vitro, EMP preferentially bound to monocytes, leading to increased CD11b expression and a 2.6-fold increase in transmigration across endothelial cells.
- Blockade of CD54 significantly reduced EMP binding to monocytes, indicating its crucial role in conjugate formation. CD54+ EMP were primarily bound to monocytes, while CD62E+ EMP were found both free and bound.
Conclusions:
- Phenotypic subsets of EMP interact differently with monocytes, with CD54 playing a key role in binding and activation.
- EMP-MoC formation enhances monocyte activation and transendothelial migration, potentially contributing to MS inflammation.
- Elevated EMP-MoC levels in MS exacerbation suggest they could serve as a sensitive biomarker for disease activity.
