RT Journal Article SR Electronic T1 CD4+ T cell-mediated immunological control of enterochromaffin cell hyperplasia and 5-hydroxytryptamine production in enteric infection JF Gut JO Gut FD BMJ Publishing Group Ltd and British Society of Gastroenterology SP 949 OP 957 DO 10.1136/gut.2006.103226 VO 56 IS 7 A1 Huaqing Wang A1 Justin Steeds A1 Yasuaki Motomura A1 Yikang Deng A1 Monica Verma-Gandhu A1 Rami T El-Sharkawy A1 John T McLaughlin A1 Richard K Grencis A1 Waliul I Khan YR 2007 UL http://gut.bmj.com/content/56/7/949.abstract AB Background: Enterochromaffin (EC) cells are dispersed throughout the gastrointestinal (GI) mucosa and are the main source of 5-hydroxytryptamine (5-HT) in the gut. 5-HT has been implicated in the pathophysiology of several GI disorders, but the mechanisms regulating 5-HT production in the gut are unknown. Aim: To investigate the role of CD4+ T cells in the production of 5-HT using a model of enteric parasitic infection. Methods and results: Severe combined immunodeficient (SCID) mice and their wild-type controls were infected with the nematode Trichuris muris and killed on various days after infection to study colonic EC cells and 5-HT production. The number of EC cells and the amount of 5-HT produced were significantly higher in infected wild-type mice than in non-infected mice. The number of EC cells and the amount of 5-HT after infection were significantly lower in SCID mice after infection than in wild-type mice. The number of EC cells and the amount of 5-HT was significantly increased after reconstitution of SCID mice with CD4+ T cells from infected mice and this was accompanied by an upregulation of colonic CD3 T cells and T helper 2 (Th2) cytokines. Laser capture microdissection-based molecular and immunofluorescence techniques revealed the presence of interleukin 13 receptor α1-chain on EC cells. Conclusion: These results show an important immunoendocrine axis in the gut, where secretory products from CD4+ T cells interact with EC cells to enhance the production of 5-HT in the gut via Th2-based mechanisms. These results show new insights into the mechanisms of gut function, which may ultimately lead to improved therapeutic strategies in functional and inflammatory disorders of the GI tract.