Immune-Endocrine Axis in Gut in Relation to Inflammation – IL13 – Serotonin

Interleukin 13 and serotonin: linking the immune and endocrine systems in murine models of intestinal inflammation.

http://www.ncbi.nlm.nih.gov/pubmed/24015275

Abstract

OBJECTIVE:

Infiltration of activated immune cells and increased cytokine production define the immunophenotype of gastrointestinal (GI) inflammation. In addition, intestinal inflammation is accompanied by alteration in the numbers of serotonin (5-hydroxytryptamine; 5-HT) synthesizing enterochromaffin (EC) cells and in 5-HT amount. It has been established that EC cells express interleukin (IL)-13 receptor, additionally IL-13 has been implicated in the pathogenesis of ulcerative colitis. In this study, we investigated the role of IL-13 mediated 5-HT signaling in pathogenesis of colitis.

METHODOLOGY:

Colitis was induced in IL-13 deficient (IL-13-/-) and wild-type (WT) mice with dextran sulfate sodium (DSS) and dinitrobenzene sulfonic acid (DNBS), as well as in IL-13-/- mice given recombinant mouse IL-13 (rmIL-13) and 5-hydroxytryptamine (5-HTP), the direct precursor of 5-HT.

PRINCIPAL FINDINGS AND CONCLUSION:

Elevated colonic IL-13 levels were observed in WT mice receiving DSS in comparison to control.

IL-13-/- mice administered DSS exhibited significantly reduced severity of colitis compared to WT mice as reflected by macroscopic and histological damage assessments.

Following DSS administration, significantly lower pro-inflammatory cytokine production and fewer infiltrating macrophages were observed in IL-13-/- mice compared to WT.

The reduced severity of colitis observed in IL-13-/- mice was also accompanied by down-regulation of EC cell numbers and colonic 5-HT content.

In addition, increasing colonic 5-HT content by administration of rmIL-13 or 5-HTP exacerbated severity of DSS colitis in IL-13-/- mice.

IL-13-/- mice also exhibited reduced severity of DNBS-induced colitis.

These results demonstrate that IL-13 plays a critical role in the pathogenesis of experimental colitis and 5-HT is an important mediator of IL-13 driven intestinal inflammation.

This study revealed important information on immune-endocrine axis in gut in relation to inflammation which may ultimately lead to better strategy in managing various intestinal inflammatory conditions including inflammatory bowel disease.

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Full Paper

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3755966/

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This entry was posted in Autism, co-morbid, Gut, Immune System, Inflammation, Mice, Physiology, Treatment. Bookmark the permalink.

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