Kazuhisa Hirayama

Platelet-Activating Factor, a Critical Mediator in the Pathogenesis of Dextran Sulfate Sodium-Induced Colitis in Rats

AbstractPURPOSE: Disorder of mucosal immunity based on an imbalance between proinflammatory and anti-inflammatory cytokines is believed to be a major factor in the pathogenesis of ulcerative colitis. Platelet-activating factor potentially stimulates the production of proinflammatory cytokines and recruits inflammatory cells. The aim of this study was to determine whether and to what extent platelet-activating factor plays a role in the pathogenesis of ulcerative colitis. METHODS: Using dextran sulfate sodium-induced colitis in rats as a model of ulcerative colitis, we analyzed the composition of cellular infiltrates and the local tissue expression of messenger ribonucleic acid for cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha. To directly assess the impact of platelet-activating factor on the development of colitis, we also determined the efficacy of a specific platelet-activating factor receptor antagonist for preventing dextran sulfate sodium-induced colitis. RESULTS: The activity of colitis was well correlated with the upregulation of cytokine-induced neutrophil chemoattractant and tumor necrosis factor-alpha messenger ribonucleic acid in local tissues and infiltration of cytokine-induced neutrophil chemoattractant-positive neutrophils and ED1-positive macrophages. The platelet-activating factor receptor antagonist effectively ameliorated colitis, along with causing a decrease in the tissue cytokine-induced neutrophil chemoattractant messenger ribonucleic acid level and a decline in neutrophil and macrophage infiltration. However, the antagonist did not alter tissue levels of tumor necrosis factor-alpha messenger ribonucleic acid. CONCLUSION: Platelet-activating factor plays a critical role in the pathogenesis of dextran sulfate sodium-induced colitis through recruitment of cytokine-induced neutrophil chemoattractant-positive neutrophils and macrophages and/or stimulation of cytokine-induced neutrophil chemoattractant release from activated neutrophils. The tissue level of tumor necrosis factor-alpha messenger ribonucleic acid does not closely reflect the activity of colitis.

Papillary endothelial hyperplasia of the liver: a case report and review of the literature.

Papillary endothelial hyperplasia (PEH) is a reactive vascular lesion that was first described by Masson in 1923 [1]. This entity is believed to be an unusual form of organizing vascular thrombus, and is characterized by anastomosing vascular channels with endothelium-lined tufts and papilla-like formations [2]. Whereas PEH occurs commonly in the vessels of the systemic soft tissues, there have been only a few case reports of PEH in the visceral organs such as kidneys [3–5] and heart [6, 7]. Here we present a case of PEH in the liver, which provided pathological findings suggesting a unique pathogenesis of the disease.