Shear forces promote lymphocyte migration across vascular endothelium bearing apical chemokines

10.1038/88710 ◽  
2001 ◽  
Vol 2 (6) ◽  
pp. 515-522 ◽  
Author(s):  
Guy Cinamon ◽  
Vera Shinder ◽  
Ronen Alon
Author(s):  
Naoki Shibuya ◽  
Masaaki Higashiyama ◽  
Yoshihiro Akita ◽  
Kazuhiko Shirakabe ◽  
Suguru Ito ◽  
...  

1972 ◽  
Vol 136 (3) ◽  
pp. 568-588 ◽  
Author(s):  
G. I. Schoefl ◽  

An electron microscope study was made of the mode of lymphocyte migration across the endothelial layer of venules in the Peyer's patches of mice and rats. Single and serial sections were examined. Of a total of about 800 lymphocytes observed in single sections, 91% were located between endothelial cells and 9% were surrounded by endothelial cytoplasm in the particular plane of section. 62% of the lymphocytes occurred in groups of two or more. In long sequences of serial sections through 21 endothelial cells, all lymphocytes were located external to the endothelial cells though some appeared "internal" at certain levels of sectioning. The probability that a lymphocyte which appears to be surrounded by endothelial cell cytoplasm actually lies within the cell was analyzed with a mathematical model derived from data obtained from single sections. The results of this analysis suggested that at least 93–99% of lymphocytes (within 90% limits of confidence) take an intercellular path in their migration from blood to lymph. It is concluded that lymphocytes migrate across the vascular endothelium by insinuating themselves between endothelial cells and not by passing through them. Rather than constituting an increased barrier to cell migration, the unusual height of the endothelial cells in these vessels is interpreted to be a special adaptation which allows sustained cell traffic without excessive fluid loss taking place concomitantly.


Blood ◽  
2004 ◽  
Vol 103 (2) ◽  
pp. 740-742 ◽  
Author(s):  
Mirjana Milinkovic ◽  
Joseph H. Antin ◽  
Charles A. Hergrueter ◽  
Charles B. Underhill ◽  
Robert Sackstein

Abstract For circulating lymphocytes to migrate to inflammatory sites, they must first adhere to the target tissue endothelium with sufficient strength to overcome the shear forces of blood flow. We previously reported that dermal papillary vessels in acute graft-versus-host disease (aGVHD) support shear-resistant lymphocyte adherence. We now identify the relevant adhesion molecule(s) directing this binding, showing that interactions between lymphocyte CD44 and hyaluronic acid (HA) expressed on dermal vessels in aGVHD alone confer this shear-resistant attachment. Native HA deposits on vascular endothelium support lymphocyte adherence, whereas HA immobilized on plastic does not. HA expressed at dermal endothelium in aGVHD is thus specialized to support lymphocyte adherence under flow conditions, and CD44-HA interactions may contribute to lymphocytotropism to skin in aGVHD.


mBio ◽  
2014 ◽  
Vol 5 (2) ◽  
Author(s):  
Katherine S. Harker ◽  
Elizabeth Jivan ◽  
Frances Y. McWhorter ◽  
Wendy F. Liu ◽  
Melissa B. Lodoen

ABSTRACT Toxoplasma gondii is a highly successful parasite that infects approximately one-third of the human population and can cause fatal disease in immunocompromised individuals. Systemic parasite dissemination to organs such as the brain and eye is critical to pathogenesis. T. gondii can disseminate via the circulation, and both intracellular and extracellular modes of transport have been proposed. However, the processes by which extracellular tachyzoites adhere to and migrate across vascular endothelium under the conditions of rapidly flowing blood remain unknown. We used microfluidics and time-lapse fluorescence microscopy to examine the interactions between extracellular T. gondii and primary human endothelial cells under conditions of physiologic shear stress. Remarkably, tachyzoites adhered to and glided on human vascular endothelium under shear stress conditions. Compared to static conditions, shear stress enhanced T. gondii helical gliding, resulting in a significantly greater displacement, and increased the percentage of tachyzoites that invaded or migrated across the endothelium. The intensity of the shear forces (from 0.5 to 10 dynes/cm2) influenced both initial and sustained adhesion to endothelium. By examining tachyzoites deficient in the T. gondii adhesion protein MIC2, we found that MIC2 contributed to initial adhesion but was not required for adhesion strengthening. These data suggest that under fluidic conditions, T. gondii adhesion to endothelium may be mediated by a multistep cascade of interactions that is governed by unique combinations of adhesion molecules. This work provides novel information about tachyzoite interactions with vascular endothelium and contributes to our understanding of T. gondii dissemination in the infected host. IMPORTANCE Toxoplasma gondii is a global parasite pathogen that can cause fatal disease in immunocompromised individuals. An unresolved question is how the parasites circulate in the body to tissues to cause disease. T. gondii parasites are found in the bloodstream of infected animals and patients, and they have been shown to adhere to and cross the endothelial cells that line blood vessel walls. To investigate these interactions, we devised a microfluidic system to visualize parasites interacting with vascular endothelium under conditions similar to those found in the bloodstream. Interestingly, parasite migration was significantly influenced by the mechanical force of shear flow. Furthermore, we identified a role for the parasite surface protein MIC2 in the initial phase of adhesion. Our study is the first to document T. gondii interactions with endothelium under shear stress conditions and provides a foundation for future studies on the molecules that mediate parasite interaction with the vasculature.


Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
A Lavaud ◽  
R Soletti ◽  
P Richomme ◽  
R Andriantsitohaina ◽  
D Guilet

1978 ◽  
Vol 39 (01) ◽  
pp. 201-209 ◽  
Author(s):  
Hiroshi Hasegawa ◽  
Hiroshi Nagata ◽  
Makoto Murao

SummaryAttempts were made to demonstrate ultrastructural changes of the tissue thromboplastin after intravenous injection, as a model experiment on the pulmonary microthrombi formation induced by the tissue thromboplastin circulating from venous return.Concentrically arranged membrane structures of the injected thromboplastin disappeared in extremely short time after the injection of the thromboplastin in rabbits. The long sheet membrane of the injected thromboplastin was frequently seen as adhered to the vascular endothelium or to the surface of blood corpuscles. Furthermore, fibrin fibres were formed in contact with the long sheet membrane of the thromboplastin. Membrane structures were not found anywhere in the control rabbits.


1989 ◽  
Vol 61 (01) ◽  
pp. 150-151 ◽  
Author(s):  
R Musso ◽  
A Longo ◽  
R R Cacciola ◽  
A Lombardo ◽  
R Giustolisi ◽  
...  

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