Special Reports and ReviewsLeukocyte-endothelial cell interactions: Molecular mechanisms and implications in gastrointestinal disease☆,☆☆
Section snippets
Molecular determinants of leukocyte adhesion
Circulating leukocytes are recruited to sites of inflammation and tissue injury by a highly coordinated and well-regulated process that largely occurs in one region of the microvasculature, i.e., postcapillary venules. Adhesion molecules expressed on the surface of endothelial cells (in postcapillary venules) and leukocytes serve to ensure an orderly sequence of cell-cell interactions that sustain leukocyte adherence to vascular endothelium and the subsequent transendothelial migration into
Leukocyte-endothelial cell adhesion in experimental models of gastrointestinal inflammation
Over the past decade, numerous studies have focused on the role of leukocytes in mediating the tissue injury that is associated with different models of acute and chronic inflammation of the gastrointestinal tract. There are now several models of gastrointestinal mucosal injury for which there is evidence that implicates a critical role for leukocyte-endothelial cell adhesion. In most of these models, evidence for the involvement of adherent leukocytes has been obtained using the technique of
Epilogue
Over the past decade, both leukocytes and endothelial cells have been implicated as active participants in the tissue injury associated with different experimental models of acute and chronic gastrointestinal inflammation. Leukocyte-endothelial cell adhesion seems to be an early and rate-limiting component of the microvascular dysfunction that accompanies these pathological conditions. The recognition that leukocyte adhesion is so critical for the inflammatory process has resulted in an
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Address requests for reprints to: D. Neil Granger, Ph.D., Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, 1501 Kings Highway, P.O. Box 33932, Shreveport, Louisiana 71130-3932. e-mail: [email protected]; fax: (318) 675-6005.
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Supported by grant SAF97-0040 from Comisión Interministerial de Ciencia y Tecnología (to J.P.) and by grants HL26441 and P01 DK43785 from the National Institutes of Health (to D.N.G.).