Changes in number of serotonin-containing cells and serotonin levels in the intestinal mucosa of rats with colitis induced by dextran sodium sulfate

Oshima, Shigeru; Fujimura, Masaki; Fukimiya, M.

doi:10.1007/s004180050445

Cited by 97 publications

(82 citation statements)

References 28 publications

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“…In addition, 5-HT content, EC cell numbers, release and SERT expression are altered in a number animal models of intestinal inflammation, including trinitro benzenesulphonic acid (TNBS) colitis 40 and ileitis 41 in guinea-pig, TNBS colitis in mouse, 42 Trichinella spiralis ileitis in mouse, 43 Citrobacter rodentium colitis in mouse 44 and dextran sodium sulphate colitis in rat 45 (see Table 5). …”

Section: Epigenetic Factorsmentioning

confidence: 99%

Review article: intestinal serotonin signalling in irritable bowel syndrome

Mawe

Coates²,

Moses

2006

Aliment Pharmacol Ther

172

137

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SUMMARYAlterations in motility, secretion and visceral sensation are hallmarks of irritable bowel syndrome. As all of these aspects of gastrointestinal function involve serotonin signalling between enterochromaffin cells and sensory nerve fibres in the mucosal layer of the gut, potential alterations in mucosal serotonin signalling have been explored as a possible mechanism of altered function and sensation in irritable bowel syndrome. Literature related to intestinal serotonin signalling in normal and pathophysiological conditions has been searched and summarized.Elements of serotonin signalling that are altered in irritable bowel syndrome include: enterochromaffin cell numbers, serotonin content, tryptophan hydroxylase message levels, 5-hydroxyindoleacedic acid levels, serum serotonin levels and expression of the serotonin-selective reuptake transporter. Both genetic and epigenetic factors could contribute to decreased serotonin-selective reuptake transporter in irritable bowel syndrome. A serotonin-selective reuptake transporter gene promoter polymorphism may cause a genetic predisposition, and inflammatory mediators can induce serotonin-selective reuptake transporter downregulation.While a psychiatric co-morbidity exists with IBS, changes in mucosal serotonin handling support the concept that there is a gastrointestinal component to the aetiology of irritable bowel syndrome. Additional studies will be required to gain a more complete understanding of changes in serotonin signalling that are occurring, their cause and effect relationship, and which of these changes have pathophysiological consequences.

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Section: Epigenetic Factorsmentioning

confidence: 99%

Review article: intestinal serotonin signalling in irritable bowel syndrome

Mawe

Coates²,

Moses

2006

Aliment Pharmacol Ther

172

137

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“…In addition to immune cells, inflammation in the intestine is associated with an alteration in the number of 5-HT-producing EC cells. Changes in the number of EC cells and 5-HT content have been observed in patients with IBD (8,9,(17)(18)(19) and also in experimental colitis (20)(21)(22). EC cells are located in very close proximity to or in contact with key immune cells (23); thus, it is very likely that 5-HT plays an important role in immune activation and generation of gut inflammation in various GI disorders including IBD.…”

mentioning

confidence: 99%

Targeted Inhibition of Serotonin Type 7 (5-HT7) Receptor Function Modulates Immune Responses and Reduces the Severity of Intestinal Inflammation

Kim

Bridle

Ghia

et al. 2013

The Journal of Immunology

108

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Mucosal inflammation in conditions ranging from infective acute enteritis or colitis to inflammatory bowel disease is accompanied by alteration in serotonin (5-hydroxytryptamine [5-HT]) content in the gut. Recently, we have identified an important role of 5-HT in the pathogenesis of experimental colitis. 5-HT type 7 (5-HT7) receptor is one of the most recently identified members of the 5-HT receptor family, and dendritic cells express this receptor. In this study, we investigated the effect of blocking 5-HT7 receptor signaling in experimental colitis with a view to develop an improved therapeutic strategy in intestinal inflammatory disorders. Colitis was induced with dextran sulfate sodium (DSS) or dinitrobenzene sulfonic acid (DNBS) in mice treated with selective 5-HT7 receptor antagonist SB-269970, as well as in mice lacking 5-HT7 receptor (5-HT7−/−) and irradiated wild-type mice reconstituted with bone marrow cells harvested from 5-HT7−/− mice. Inhibition of 5-HT7 receptor signaling with SB-269970 ameliorated both acute and chronic colitis induced by DSS. Treatment with SB-269970 resulted in lower clinical disease, histological damage, and proinflammatory cytokine levels compared with vehicle-treated mice post-DSS. Colitis severity was significantly lower in 5-HT7−/− mice and in mice reconstituted with bone marrow cells from 5-HT7−/− mice compared with control mice after DSS colitis. 5-HT7−/− mice also had significantly reduced DNBS-induced colitis. These observations provide us with novel information on the critical role of the 5-HT7 receptor in immune response and inflammation in the gut, and highlight the potential benefit of targeting this receptor to alleviate the severity of intestinal inflammatory disorders such as inflammatory bowel disease.

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“…One of the widely used experimental models resembling human ulcerative colitis has been developed by treatment of animals with dextran sulfate sodium (DSS 1 ) in drinking water for 6 to 10 days (Okayasu et al, 1990). Because DSS is a large and negatively charged molecule that cannot easily cross the membranes, it is poorly absorbed after oral administration (Lorentsen et al, 1989;Oshima et al, 1999). Thus, it is generally accepted that DSS exerts its effects on the luminal surface of the colonic mucosa (Okayasu et al, 1990;Ni et al, 1996).…”

mentioning

confidence: 99%

Endotoxin-Mediated Disturbance of Hepatic Cytochrome P450 Function and Development of Endotoxin Tolerance in the Rat Model of Dextran Sulfate Sodium-Induced Experimental Colitis

Masubuchi¹,

Horie²

2004

Drug Metab Dispos

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ABSTRACT:Hepatobiliary abnormalities have been described in patients with chronic inflammatory bowel diseases. Hepatic cytochrome P450 (P450)-dependent drug-metabolizing enzyme activities and susceptibility to a hepatotoxin, D-galactosamine, were determined in rats with dextran sulfate sodium (DSS)-induced colitis to assess whether liver function is affected in the model of inflammatory bowel disease. Colitis was induced by treatment of rats with 3% DSS in drinking water for 7 days. Liver microsomes for enzyme activities and serum for biological analysis were prepared from the rats with colitis, along with untreated and lipopolysaccharide (LPS)-treated rats. Other rats received intraperitoneal injection of D-galactosamine to assess their susceptibility to the toxin-induced liver injury. Treatment of rats with DSS resulted in not only colitis but also decreases in hepatic P450-dependent drug-metabolizing enzyme activities. Elevated endotoxin was found in portal blood, which was not associated with liver injury. The potency and the isoform selectivity in the suppression of the P450 enzymes by DSS treatment were similar to those of LPS-treated rats. Coadministration of antibiotics, polymyxin B or metronidazole, with DSS protected rats from decreases in some but not all P450 enzyme activities, indicating partial involvement of bacterial endotoxin in the P450 decreases. The rats with colitis were less susceptible than untreated rats to D-galactosamine-induced liver injury and TNF-␣ production, suggesting development of endotoxin tolerance in DSS-colitis. In conclusion, these results suggest that the DSScolitis leads to endotoxin-mediated down-regulation of hepatic P450 enzymes and protection against D-galactosamine-induced liver injury, probably due to endotoxin tolerance.

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Changes in number of serotonin-containing cells and serotonin levels in the intestinal mucosa of rats with colitis induced by dextran sodium sulfate

Cited by 97 publications

References 28 publications

Review article: intestinal serotonin signalling in irritable bowel syndrome

Review article: intestinal serotonin signalling in irritable bowel syndrome

Targeted Inhibition of Serotonin Type 7 (5-HT7) Receptor Function Modulates Immune Responses and Reduces the Severity of Intestinal Inflammation

Endotoxin-Mediated Disturbance of Hepatic Cytochrome P450 Function and Development of Endotoxin Tolerance in the Rat Model of Dextran Sulfate Sodium-Induced Experimental Colitis

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