| Title | Differential regulation of eosinophil adhesion under conditions of flow in vivo. | | Author(s) | Sriramarao P, Broide DH | | Institution | Laboratory of Immunology and Vascular Biology, La Jolla Institute for Experimental Medicine, California 92037, USA. | | Source | Ann N Y Acad Sci 1996 Oct 31.:218-25. | | MeSH | Animals
Anti-Allergic Agents
Blood Flow Velocity
Cell Adhesion
Chemotaxis, Leukocyte
Endothelium, Vascular
Eosinophils
Humans
Integrin alpha4beta1
Integrins
L-Selectin
Rabbits
Receptors, Lymphocyte Homing
Receptors, Very Late Antigen
Research Support, U.S. Gov't, P.H.S.
| | Abstract | The proinflammatory role of eosinophils in patients with allergic inflammation is now well recognized. However, the molecular mechanisms mediating the sequential events of eosinophil recruitment from the blood stream to sites of allergic inflammation under conditions of shear force have not been clearly established. Using the xenogeneic rabbit model system to study human eosinophil adhesion under conditions of flow in vivo, we have demonstrated that eosinophils like neutrophils roll, adhere, and extravasate across cytokine-stimulated endothelial cells at physiological shear rates in vivo. Eosinophils rolling on venular endothelial cells is mediated by L-selectin and VLA-4. Mediators of cellular activation such as GM-CSF, PAF, or PMA had a differential effect on neutrophil and eosinophil receptor expression and their rolling function. It would thus appear that acting sequentially or in concert a variety of cytokines, including GM-CSF, RANTES, IL-5, and specific cell adhesion molecules (VLA-4/VCAM-1) might play a critical role in the selective sequestration of eosinophils and other proinflammatory leukocytes into the inflamed tissues during episodes of allergic inflammation. Further understanding of the function of these mediators as well as other traffic signals that regulate eosinophil adhesion will help in developing better therapeutic strategies to block the emigration of eosinophils from the blood stream, and also to inhibit the activation of eosinophils once they have reached sites of tissue inflammation. | | Language | eng | | Pub Type(s) | Journal Article
Review
| | PubMed ID | 8906229 |
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