36 research outputs found
Somatostatin Inhibits the Production of Interferon-γ by Intestinal Epithelial Cells During Intestinal Ischemia–Reperfusion in Macaques
Potential immunological consequences of pharmacological suppression of gastric acid production in patients with multiple sclerosis
Corticosteroids are standard treatment for patients with multiple sclerosis experiencing acute relapse. Because dyspeptic pain is a common side effect of this intervention, patients can be given a histamine receptor-2 antagonist, proton pump inhibitor or antacid to prevent or ameliorate this disturbance. Additionally, patients with multiple sclerosis may be taking these medications independent of corticosteroid treatment. Interventions for gastric disturbances can influence the activation state of the immune system, a principal mediator of pathology in multiple sclerosis. Although histamine release promotes inflammation, activation of the histamine receptor-2 can suppress a proinflammatory immune response, and blocking histamine receptor-2 with an antagonist could shift the balance more towards immune stimulation. Studies utilizing an animal model of multiple sclerosis indicate that histamine receptor-2 antagonists potentially augment disease activity in patients with multiple sclerosis. In contrast, proton pump inhibitors appear to favor immune suppression, but have not been studied in models of multiple sclerosis. Antacids, histamine receptor-2 antagonists and proton pump inhibitors also could alter the intestinal microflora, which may indirectly lead to immune stimulation. Additionally, elevated gastric pH can promote the vitamin B12 deficiency that patients with multiple sclerosis are at risk of developing. Here, we review possible roles of gastric acid inhibitors on immunopathogenic mechanisms associated with multiple sclerosis
Mast Cells as Targets for the Therapy of Inflammatory Bowel Disease
The etiology and pathogenesis of inflammatory bowel disease
(IBD) is poorly understood. However, numerous studies have demonstrated that
immunological and inflammatory responses are activated during this disease. A
better understanding of these events will help identify appropriate therapeutic
interventions. Mast cell hyperplasia is a prominent feature of inflamed intestinal
tissue in IBD. Intestinal mast cells are heterogeneous and at least two populations
are present in the human intestine. The authors' objective is to explore mast cell
properties, activation and mediators that are involved in the induction, maintenance
and perpetuation of inflammatory lesions in the intestine. Although
some therapies used in IBD can modulate mast cell activities, whether these
actions are important in the beneficial effects of the drugs is unknown. Future
drug development targeted to the inhibition of mast cells might be of therapeutic
value. However, a cascade of different cellular events are involved in IBD
development. The complexity of the disease raises difficulties in the development
of therapies. Multiple drugs, selective for different phases of the disease or acting
on different cells, might be most appropriate, rather than a single, all-encompassing
therapeutic agent