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Journal of Blood Disorders Symptoms and Treatments

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Research Article

Microparticles from Children with Sickle Cell Anemia and the Acute Chest Syndrome Cause Activation of Human Pulmonary Endothelium

Christopher McKinney, Marguerite R Kelher, Rachelle Nuss, Alysse Cool, Alex Hoffman, Christopher C Silliman

Correspondence Address :

Christopher C Silliman
MD, PhD, Senior Independent Investigator
Research Laboratory
Bonfils Blood Center
717 Yosemite Street, Denver, CO 80230, USA
Email: Christopher.Silliman@ucdenver.edu

Received on: February 28, 2018, Accepted on: March 09, 2018, Published on: March 16, 2018

Citation: Christopher McKinney, Marguerite R Kelher, Rachelle Nuss, et al. (2018) Microparticles from Children with Sickle Cell Anemia and the Acute Chest Syndrome Cause Activation of Human Pulmonary Endothelium

Copyright: 2018 Christopher C Silliman et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

  • Abstract

Abstract
Children with sickle cell anemia (SCA) have increased numbers of microparticles (MPs) some of which increase with known SCA complications. Statins have pleiotropic effects including inhibition of MP formation. We hypothesize that MPs increase in children with SCA, depending upon their disease state, and cause pro-inflammatory activation of vascular endothelium which is statin-inhibitable. Blood was drawn from children with SCA at clinic, when they were well (resting) and upon hospital admission for vaso-occlusive crisis (VOC) or with the acute chest syndrome (ACS). MPs were isolated by centrifugation and classified with fluorescently-labelled antibodies and flow cytometry. Pulmonary human microvascular endothelial cells (HMVECs) were incubated with MPs and intercellular adhesion molecule-1 (ICAM-1) surface expression measured by flow cytometry with chemokine release measured by ELISA. VOC caused increased red blood cell (RBCs) plasma MPs, while ACS induced increased MPs from platelets, leukocytes, and RBCs versus resting samples.
The MPs from ACS elicited increased HMVEC ICAM-1 surface expression and release of IL-8 and growth-related oncogene- α (Gro-α). Simvastatin abrogated HMVEC activation. We conclude that VOC and ACS increase plasma MP formation, and the ACS MPs caused pro-inflammatory activation of HMVECs that were statin-inhibitable. Statin treatment may decrease ACS, and a clinical trial is warranted.

Keywords: Intercellular adhesion molecule-1, Interleukin-8, Growth-related oncogene-α, Statins

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