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Mol Immunol. 2012 Feb;50(1-2):117-23. doi: 10.1016/j.molimm.2011.12.012. Epub 2012 Jan 20.

Monocytes from sickle cell disease patients induce differential pulmonary endothelial gene expression via activation of NF-κB signaling pathway.

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  • 1Center of Excellence in Sickle Cell Disease and Division of Hematology/Oncology, Department of Medicine, Boston University School of Medicine, 88-East Newton St., Boston, MA 02118, USA.


Monocyte-endothelial interactions play an important role in inflammatory diseases and may modulate vasculopathy in sickle cell disease, a disorder with an important inflammatory component. We co-incubated normal and sickle monocytes, lymphocytes and TNF-α with pulmonary microvascular and arterial endothelial cells and compared the expression of genes coding for adhesion molecules and cytokines that might contribute to sickle vasoocclusion. Monocyte-endothelial cell co-incubation resulted in up-regulation of L-selectin, E-selectin, VCAM-1, ICAM-1, MCP-1, MMP-1, TNF-α, IL-6 and IL-1β and down-regulation of eNOS. Lymphocyte-endothelial cell co-incubations, induced similar effects restricted to pulmonary artery endothelial cells. TNF-α had similar effects on the endothelial cells as monocytes did, however monocyte induced gene expression in endothelial cells was not TNF-α dependent but was regulated through the NF-κB pathway. Sickle monocytes lead to altered expression of L-selectin, MCP-1 and MMP-1 in pulmonary vascular endothelium when compared with normal monocytes. The gene expression changes we observed could reflect pathological events of sickle vasoocclusion.

Copyright © 2012 Elsevier Ltd. All rights reserved.

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