Enterochromaffin cell hyperplasia and decreased serotonin transporter in a mouse model of postinfectious bowel dysfunction

Neurogastroenterology and Motility - Tập 17 Số 6 - Trang 863-870 - 2005
Johanna Wheatcroft1, D. Wakelin2, Adrian L. Smith3, Christine R. Mahoney4, Gary M. Mawe4, Robert E. Spiller5
1Wolfson Digestive Diseases Centre, University Hospital, Nottingham, UK.
2Department of Life Sciences, University Hospital, Nottingham, UK
3Division of Immunology and Pathology, Institute of Animal Health, Compton, Berkshire, UK
4Department of Anatomy and Neurobiology, University of Vermont, Burlington, Vermont, USA
5Wolfson Digestive Diseases Centre, University Hospital, Nottingham &

Tóm tắt

Abstract  Patients with postinfective irritable bowel syndrome and Trichinella spiralis‐infected mice share many features including visceral hypersensitivity and disordered motility. We assessed enterochromaffin (EC) numbers and serotonin transporter (SERT) using National Institute of Health (NIH) female mice studied for up to 56 days post‐T. spiralis infection. The effects of steroid treatment and the T‐cell dependence of the observed responses were assessed by infection of hydrocortisone‐treated or T‐cell receptor knock out [TCR (β×δ) KO] animals. Enterochromaffin cell density in uninfected animals increased from duodenum 10.0 cells mm−2 (5.9–41.0) to colon 61.8. (46.3–162) cells mm−2P < 0.0001. Infection increased duodenal and jejunal counts which rose to 37.3 (22–57.7) cells mm−2 and 50.6 (7–110.8) cells mm−2, respectively, at day 14. Infection significantly reduced jejunal SERT expression, with luminance values falling from 61.0 (45.1–98.3) to a nadir of 11.6 (0–36.0) units at day 9, P < 0.001. Specific deficiencies in all T cells reduced EC hyperplasia and abrogated infection‐induced mastocytosis. Thus infection induced inflammation increases EC numbers, as has been reported in PI‐IBS, and reduces SERT. This may increase mucosal 5HT availability and contribute to the clinical presentation of PI‐IBS.

Từ khóa


Tài liệu tham khảo

10.1136/gut.44.3.400

10.1136/gut.2003.021154

10.1111/j.1572-0241.2003.07542.x

10.1053/j.gastro.2003.09.028

10.1046/j.1365-2036.2003.01640.x

10.1053/gast.2002.33584

10.1053/j.gastro.2004.04.006

Collins SM, 1989, Impaired acetylcholine release from the myenteric plexus of Trichinella‐infected rats, Am J Physiol, 257, G898

10.1016/0016-5085(91)90456-U

10.1152/ajpgi.00488.2002

10.1136/gut.47.6.804

10.1017/S0031182000079816

10.1051/parasite/200108s2110

10.1152/ajpgi.00090.2004

10.1053/j.gastro.2004.03.013

10.1523/JNEUROSCI.15-02-01261.1995

10.1523/JNEUROSCI.16-07-02352.1996

10.1152/ajpgi.00090.2004

10.1016/S0016-5085(83)80080-8

10.1111/j.1365-3024.1993.tb00572.x

10.1136/gut.2003.035451

Valance BA, 1997, Increased intestinal muscle contractility and worm expulsion in nematode‐infected mice, Am J Physiol, 272, G321

10.1017/S0031182000048472

10.1111/j.1572-0241.2003.08669.x

10.1136/gut.53.1.78

10.1053/gast.2002.37055

10.1136/gut.52.4.523

10.2307/3273810

10.1046/j.1365-2249.2001.01589.x

Thông tin
Thông tin xuất bản

Neurogastroenterology and Motility

Tập 17 Số 6

863-870

Thông tin tác giả