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International Immunology Advance Access originally published online on December 21, 2007
International Immunology 2008 20(2):247-257; doi:10.1093/intimm/dxm136
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© The Author 2007. Published by Oxford University Press on behalf of The Japanese Society for Immunology. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press and The Japanese Society for Immunology are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

LPS differentially regulates adhesion and transendothelial migration of human monocytes under static and flow conditions

Paul F. Bradfield1, Caroline A. Johnson-Léger1,2, Claudia Zimmerli1 and Beat A. Imhof1

1 Department of Pathology and Immunology, University Medical Centre, 1 Rue Michel-Servet, CH-1211 Geneva 4, Switzerland
2 Present address: Merck Serono International S.A., 9 chemin des Mines, 1202 Geneva, Switzerland

Correspondence to: B. A. Imhof; E-mail: beat.imhof{at}medecine.unige.ch

One of the key components of the innate immune response is the recognition of microbial products such as LPS by Toll-like receptors on monocytes and neutrophils. We show here that short-term stimulation of primary human monocytes with LPS led to an increase in adhesion of monocytes to endothelial cells and a dramatic decrease in transendothelial migration under static conditions. In contrast, under normal physiological flow, monocyte adhesion and migration across a human umbilical vein endothelial cell monolayer appeared to be unaffected by LPS treatment. LPS stimulation of monocytes activated β1 and β2 integrins, but did not increase their surface expression levels. During septic shock, reduction in blood flow as a result of vasodilation and vascular permeability leads to adhesion and accumulation of LPS-stimulated circulating monocytes onto the blood vessel walls. The different findings of monocyte migration under static and flow conditions in our study may offer one explanation for this phenomenon. The rapid engagement of LPS-activated monocytes preventing transendothelial migration could represent a novel mechanism of bacterial exclusion from the vasculature. This occurs during the early stages of sepsis, and in turn may modulate the severity of the pathophysiology.

Keywords: flow, leukocytes, LPS, monocytes, transendothelial migration

Transmitting editor: M. Miyasaka

Received 17 August 2007, accepted 25 November 2007.


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