The role of junctional adhesion molecule C (JAM-C) in acute pancreatitis

Autor: Beat A. Imhof, Alain Vonlaufen, Catherine M. Pastor, Michel Aurrand-Lions, Jean-Louis Frossard, Antoine Hadengue, Chrystelle Lamagna
Rok vydání: 2006
Předmět:
Necrosis
Pancreas/immunology/pathology
Immunoglobulins/immunology/ physiology
ddc:616.07
Mice
Immunohistochemistry/methods
Edema
Cell adhesion molecule
Antibodies
Monoclonal
Immunohistochemistry
humanities
Caerulein
Chemotaxis
Leukocyte
Acute Disease
Amylases
Models
Animal
cardiovascular system
Acute pancreatitis
medicine.symptom
Junctional Adhesion Molecule C
Ceruletide
Blotting
Western
Immunoglobulins
Inflammation
Antibodies
Monoclonal/therapeutic use
Mice
Transgenic
Amylases/blood
Pancreatitis/blood/ metabolism/pathology
Cell Adhesion Molecules/immunology/ physiology
Endothelial Cells/ metabolism/pathology
Pathology and Forensic Medicine
Proinflammatory cytokine
medicine
Acinar cell
Blotting
Western/methods
Animals
Pancreas
business.industry
Interleukin-6
fungi
Endothelial Cells
Membrane Proteins
Membrane Proteins/immunology/ physiology
medicine.disease
Mice
Inbred C57BL
Pancreatitis
Immunology
Cancer research
Interleukin-6/blood
business
Cell Adhesion Molecules
Zdroj: The Journal of Pathology, Vol. 209, No 4 (2006) pp. 540-548
ISSN: 0022-3417
Popis: The recruitment of inflammatory cells contributes significantly to tissue injury in acute pancreatitis. This process implies several molecular interactions between circulating and endothelial cells. The adhesion molecule junctional adhesion molecule C (JAM-C) is involved in leukocyte transendothelial migration and it can form homophilic (JAM-C/JAM-C) and heterophilic interactions with the leukocyte integrin alpha(M)beta(2). In this study, the effect of early administration of monoclonal antibodies directed against JAM-C in cerulein-induced acute pancreatitis was assessed. This reagent significantly blocked influx of leukocytes, release of serum amylase, secretion of inflammatory cytokines, and acinar cell necrosis. These effects were rapid and protected against tissue injury throughout the duration of the model. Conversely, cerulein-induced acute pancreatitis was more severe in transgenic mice overexpressing JAM-C on endothelial cells under the control of the Tie2 promoter. It is proposed that JAM-C expressed by endothelial cells contributes to the pathophysiology of acute pancreatitis and could be considered a target for clinical applications.
Databáze: OpenAIRE
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