Somatostatin in inflammatory bowel disease

Abstract

Intestinal in ammation is controlled by various immunomodulating cells, interacting by molecular mediators. Neuropeptides, released by enteric nerve cells and neuroendocrine mucosa cells, are able to affect several aspects of the general and intestinal immune system, with both pro-as well as anti-in ammatory activities. In in ammatory bowel disease (IBD) there is both morphological as well as ex perimental evidence for involvement of neuropeptides in the pathogenesis. Somatostatin is the main inhibitory peptide in in ammatory processes, and its possible role in IBD is discussed.

Effects of octreotide treatment on early TNF‐α production and localization in experimental chronic colitis

“…44 Octreotide possesses anti-TNFa properties in leucocytes and vascular cells. 15,16,18,45 Our data, showing that octreotide attenuates TNFa immunostaining in muscle layers, suggest that the anti-in¯ammatory properties of octreotide also occur in smooth muscle cells. Five subtypes of somatostatin receptors have been cloned.…”

Double benefit of long-acting somatostatin analogs in a patient with coexistence of acromegaly and ulcerative colitis

“…15 Somatostatin is the main inhibitory peptide in inflammatory bowel disease. 37 This is the first case report of an association between UC and acromegaly. Interestingly, when the somatostatin analog was initiated as primary treatment for acromegaly, we observed improvement in both diseases.…”

“…This loss of SMS production correlates with disease activity in experimental colitis . Somatostatin is the main inhibitory peptide in inflammatory bowel disease …”

Somatostatin receptor expression in the ileal mucosa of patients with inflammatory bowel disease

“…Большинство проведенных ранее исследований было направлено на анализ клеток, продуцирующих соматостатин, а не экспрессирующих РС [2,4]. В этих работах было выявлено, что при ВЗК, особенно у больных с ЯК, значительно уменьшается число соматостатинсодержащих клеток преимущественно в дистальных отделах ободочной кишки.…”

“…Полагают, что причиной ВЗК является патологическая реакция иммунной системы в ответ на воздействие микроорганизмов на слизистую оболочку кишечника у генетически предрасположенных лиц [1]. В патогенезе ВЗК обсуждаются значение нейроэндокринно-иммунных взаимодействий и нарушения регуляторной деятельности диффузной эндокринной системы кишечника, в частности была показана роль соматостатина как одного из нейропептидов с противовоспалительным действием [2][3][4].…”