Activated platelets in ulcerative colitis enhance the production of reactive oxygen species by polymorphonuclear leukocytes

Citation
K. Suzuki et al., Activated platelets in ulcerative colitis enhance the production of reactive oxygen species by polymorphonuclear leukocytes, SC J GASTR, 36(12), 2001, pp. 1301-1306
Citations number
43
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
ISSN journal
00365521 → ACNP
Volume
36
Issue
12
Year of publication
2001
Pages
1301 - 1306
Database
ISI
SICI code
0036-5521(200112)36:12<1301:APIUCE>2.0.ZU;2-N
Abstract
Background: Although the number of activated platelets increases in the per ipheral blood of patients with inflammatory bowel disease (IBD), the role o f activated platelets in the polymorphonuclear leukocytes (PMN)-mediated mu cosal injury in IBD remains unclear. In the present study, we used luminol- enhanced chemiluminescence (LCL) to examine the influence of platelets from patients with ulcerative colitis (UC) on the production of reactive oxygen species EROS) by circulating PMN. Methods: The proportion of P-selectin-po sitive activated platelets was determined using flow cytometry. PMN from pa tients with UC and normal controls were stimulated using phorbol 12-myrista te 13-acetate with or without autologous platelets, anti-P-selectin monoclo nal antibody and thrombin. Indicator PMN from a normal volunteer were stimu lated using heterologous platelets from UC patients and normal controls, an d LCL signals were registered every 60 see for 240 min. Results: The propor tion of activated platelets was significantly increased in IBD patients. Th e level of ROS production by PMN did not significantly differ between UC pa tients and normal controls in the absence of a platelet-PMN interaction. Pl atelets from UC patients enhanced the amount of ROS produced by indicator P MN significantly more than those from normal controls. This effect was part ly diminished by anti-P-selectin monoclonal antibody. Conclusions: Platelet activation in UC might be responsible for the secondary activation of PMN, which could account for the increase in PMN-mediated tissue injury associa ted with UC.