Antral Somatostatin Contents and Acidity of Gastric Juice in Normal Subjects and Patients with Duodenal Ulcer

The antral somatostatin contents were investigated in biopsy specimens of the antrum from normal subjects and patients with duodenal ulcer. There was good correlation (r=0.77044) between antral somatostatin contents and maximal acidity in normal subjects, but the correlation between antral somatostatin contents and maximal acid output was not significant (r=0.254367). This result may indicate that antral somatostatin content is regulated by intragastric pH in normal subjects. On the other hands, no correlation was observed between antral somatostatin contents and acidity or acid output in patients with duodenal ulcer. Therefore the impaired regulation of acid on antral somatostatin contents could be one of the important factors in the pathogenesis of duodenal ulcer disease

Synthetic retinoid Am80 ameliorates chronic graft-versus-host disease by down-regulating Th1 and Th17.

Chronic GVHD (cGVHD) is a main cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the roles of Th subsets in cGVHD with the use of a well-defined mouse model of cGVHD. In this model, development of cGVHD was associated with up-regulated Th1, Th2, and Th17 responses. Th1 and Th2 responses were up-regulated early after BM transplantation, followed by a subsequent up-regulation of Th17 cells. Significantly greater numbers of Th17 cells were infiltrated in the lung and liver from allogeneic recipients than those from syngeneic recipients. We then evaluated the roles of Th1 and Th17 in cGVHD with the use of IFN-γ-deficient and IL-17-deficient mice as donors. Infusion of IFN-γ(-/-) or IL-17(-/-) T cells attenuated cGVHD in the skin and salivary glands. Am80, a potent synthetic retinoid, regulated both Th1 and Th17 responses as well as TGF-β expression in the skin, resulting in an attenuation of cutaneous cGVHD. These results suggest that Th1 and Th17 contribute to the development of cGVHD and that targeting Th1 and Th17 may therefore represent a promising therapeutic strategy for preventing and treating cGVHD