HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ramudo, L. Articles by Manso, M. A. Search for Related Content PubMed PubMed Citation Articles by Ramudo, L. Articles by Manso, M. A.

---

ORIGINAL RESEARCH ARTICLE

ICAM-1 and CD11b/CD18 Expression During Acute Pancreatitis Induced by Bile-Pancreatic Duct Obstruction: Effect of N-Acetylcysteine

Laura Ramudo^*, Isabel De Dios^*,1, Sara Yubero^*, Secundino Vicente and Manuel A. Manso^*

^* Department of Physiology and Pharmacology and Department of Toxicology, University of Salamanca, 37007 Salamanca, Spain

To whom requests for reprints should be addressed at ¹ Departamento de Fisiologia y Farmacologia, Edificio Departamental, Campus Miguel de Unamuno, 37007 Salamanca, Spain. E-mail: bel{at}usal.es

Different molecules are involved in the recruitment of leukocytes during inflammation. The aim was to investigate (i) the contribution of acinar cells to the overall production of ICAM-1 and (ii) the kinetics of leukocyte CD11b/CD18 expression during acute pancreatitis (AP) induced by bile-pancreatic duct obstruction (BPDO) to evaluate the contribution of both molecules to leukocyte homing. The role of reactive oxygen species (ROS) as mediators in the expression of ICAM-1 and CD11b/CD18 was examined by using N-acetylcysteine (NAC) as an antioxidant treatment. By mechanisms resistant to NAC treatment, acinar cells were able to produce ICAM-1 at first onset of AP; other cell sources contribute to maintaining increased ICAM-1 plasma levels during AP. By contrast, CD11b/CD18 was overexpressed in leukocytes in the course of AP by oxidant-dependent mechanisms. Since NAC treatment reduced neutrophil infiltration in the pancreas, we conclude that CD11b/CD18 over-expression is required for leukocyte recruitment; however, other adhesion molecules in addition to ICAM-1 seem to contribute to leukocyte homing during BPDO-induced AP.

Key Words: acute pancreatitis • adhesion molecules • ß₂-integrins • CD11b/CD18 • ICAM-1 • reactive oxygen species

This article has been cited by other articles:

				A. Y. Meliton, N. M. Munoz, X. Zhu, and A. R. Leff Attenuated translocation of group IVa phospholipase A2 and up-regulated annexin-1 synthesis by glucocorticoid blocks {beta}2-integrin adhesion in neutrophils J. Leukoc. Biol., February 1, 2008; 83(2): 344 - 351. [Abstract] [Full Text] [PDF]