Mechanisms of platelet and leukocyte recruitment in experimental colitis

Both leukocytes and platelets accumulate in the colonic microvasculature during experimental colitis, leading to microvascular dysfunction and tissue injury. The objective of this study was to determine whether the recruitment of leukocytes and platelets in inflamed colonic venules are codependent p...

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Bibliographic Details
Published in:American journal of physiology: Gastrointestinal and liver physiology 2007-11, Vol.293 (5), p.G1054-G1060
Main Authors: Vowinkel, Thorsten, Wood, Katherine C, Stokes, Karen Y, Russell, Janice, Tailor, Anitaben, Anthoni, Christoph, Senninger, Norbert, Krieglstein, Christian F, Granger, D Neil
Format: Article
Language:English
Subjects:
Animals
Blood clots
Blood Platelets - physiology
Colitis - blood
Colitis - physiopathology
Disease Models, Animal
Endothelium, Vascular - physiology
Gastroenterology
Inflammatory bowel disease
Leukocytes
Leukocytes - physiology
Male
Mice
Mice, Inbred C57BL
Proteins
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Summary:Both leukocytes and platelets accumulate in the colonic microvasculature during experimental colitis, leading to microvascular dysfunction and tissue injury. The objective of this study was to determine whether the recruitment of leukocytes and platelets in inflamed colonic venules are codependent processes. The rolling and adherence of leukocytes and platelets in colonic venules of mice with dextran sodium sulfate (DSS)-induced colitis were monitored by intravital videomicroscopy. DSS elicited an increased recruitment of both rolling and adherent leukocytes and platelets. DSS-colitic mice rendered thrombocytopenic with anti-platelet serum exhibited profound reductions in leukocyte adhesion. Neutropenia, induced with anti-neutrophil serum, significantly reduced the adhesion of leukocytes and the accumulation of platelet-leukocyte aggregates while greatly enhancing the number of platelets that roll and adhere directly to venular endothelial cells. The enhanced platelet adhesion associated with neutropenia was mediated by platelet P-selectin interactions with endothelial cell P-selectin glycoprotein ligand (PSGL-1). DSS colitis was also associated with an increased expression of PSGL-1 in the colonic vasculature. These findings indicate that the recruitment of leukocytes and platelets in inflamed colonic venules are co-dependent processes.
ISSN:0193-1857
1522-1547
DOI:10.1152/ajpgi.00350.2007