Mechanisms underlying the promotion of 5‐hydroxytryptamine secretion in enterochromaffin cells of constipation mice by Bifidobacterium and Lactobacillus

Serotonin (5-HT), predominantly synthesized and released by enterochromaffin cells, is implicated in gastrointestinal symptoms such as emesis, abdominal pain, and diarrhea. Because luminal short-chain fatty acids (SCFAs) release 5-HT from enterochromaffin cells, which express the SCFA receptor free fatty acid receptor 2 (FFA2) in rat duodenum, we examined the effects of the selective FFA2 agonist phenylacetamide-1 (PA1) on duodenal 5-HT release with consequent bicarbonate secretion [duodenal bicarbonate secretion (DBS)] and on indomethacin (IND)-induced enteropathy. Intestinal injury was induced by IND (10 mg/kg sc) with or without PA1. We measured DBS in vivo in a duodenal loop perfused with PA1 while measuring 5-HT released in the portal vein. Duodenal blood flow was measured by laser-Doppler flowmetry. IND induced small intestinal ulcers with duodenal sparing. PA1 given with IND (IND + PA1) dose dependently induced duodenal erosions. IND + PA1-induced duodenal lesions were inhibited by the FFA2 antagonist GLPG-0974, ondansetron, or omeprazole but not by RS-23597 or atropine. Luminal perfusion of PA1 augmented DBS accompanied by increased portal blood 5-HT concentrations with approximately eight times more release at 0.1 mM than at 1 µM, with the effects inhibited by coperfusion of GLPG-0974. Luminal PA1 at 1 µM increased, but at 0.1 mM diminished, duodenal blood flow. Cosuperfusion of PA1 (0.1 mM) decreased acid-induced hyperemia, further reduced by IND pretreatment but restored by ondansetron. These results suggest that, although FFA2 activation enhances duodenal mucosal defenses, FFA2 overactivation during ulcerogenic cyclooxygenase inhibition may increase the vulnerability of the duodenal mucosa to gastric acid via excessive 5-HT release and 5-HT3receptor activation, implicated in foregut-related symptoms such as emesis and epigastralgia.NEW & NOTEWORTHY Luminal free fatty acid receptor 2 agonists stimulate enterochromaffin cells and release serotonin, which enhances mucosal defenses in rat duodenum. However, overdriving serotonin release with high luminal concentrations of free fatty acid 2 ligands such as short-chain fatty acids injures the mucosa by decreasing mucosal blood flow. These results are likely implicated in serotonin-related dyspeptic symptom generation because of small intestinal bacterial overgrowth, which is hypothesized to generate excess SCFAs in the foregut, overdriving serotonin release from enterochromaffin cells.

Download Full-text

Fe II uptake of enterochromaffin Biochemical and histochemical study of the ferrous ion uptake reaction in relation to enterochromaffin cells and mast cells

Acta Histochemica ◽

10.1016/s0065-1281(78)80071-3 ◽

1978 ◽

Vol 61 (2) ◽

pp. 248-256 ◽

Cited By ~ 1

Author(s):

Ralph D. Lillie ◽

Patricia T. Donaldson ◽

Philip Pizzolato ◽

Columbia Reynolds ◽

Shitalkumar Jirge

Keyword(s):

Mast Cells ◽

Histochemical Study ◽

Enterochromaffin Cells ◽

Ion Uptake ◽

Ferrous Ion

Download Full-text

Peutz-Jeghers syndrome: Quantitative study on enterochromaffin cells in hamartomatous intestine polyps

Srpski arhiv za celokupno lekarstvo ◽

10.2298/sarh1310602k ◽

2013 ◽

Vol 141 (9-10) ◽

pp. 602-607

Author(s):

Miljan Krstic ◽

Vuka Katic ◽

Slavica Stojnev ◽

Dragan Mihailovic ◽

Marijola Mojsilovic ◽

...

Keyword(s):

Clinical Manifestations ◽

Enterochromaffin Cells ◽

Ileal Mucosa ◽

Cell Hyperplasia ◽

Ki 67 ◽

Intestinal Polyps ◽

Serotonin Secretion ◽

Formalin Fixed Paraffin Embedded ◽

Ec Cells ◽

Peutz Jeghers Syndrome

Introduction. Peutz-Jeghers (PJ) syndrome is a rare familial disorder with the autosomal transmission characterized by multiple intestinal polyps, mucocutaneous pigmentation and increased incidence of various malignancies. Some clinical manifestations of PJ syndrome may be associated with the serotonin secretion from the enterochromaffin cells (EC). Objective. Since no data have been reported so far regarding EC cells in PJ polyps, the aim of our study was to quantitatively investigate EC population in hamartomatous intestinal polyps in patients with the PJ syndrome. Methods. The samples of surgically removed PJ polyps from family members with the PJ syndrome were collected during 34-year follow-up period. Formalin-fixed paraffin-embedded specimens of twenty-one PJ polyps were stained with HE, AB-PAS, Van Gieson, Fontana-Masson, FIF and Grimelius. For immuno- histochemical analysis, the following antibodies were used: chromogranin A, serotonin, Ki-67, desmin, vimentin and cytokeratin in order to eliminate differential diagnostic possibilities and to confirm diagnosis of PJ polyps. Results. Strong EC cell hyperplasia was observed within the tissue of the investigated polyps. Statistical analysis demonstrated significantly higher content of EC cells in PJ polyps than in the normal ileal mucosa. Conclusion. Marked hyperplasia of EC cells within the PJ polyps may be the most important contributor to functional disorders in patients with the PJ syndrome.

Download Full-text

Indole reactions of mast cells and enterochromaffin cells related to fixations with and without aldehydes

Histochemistry ◽

10.1007/bf00495763 ◽

1978 ◽

Vol 55 (3) ◽

pp. 245-250

Author(s):

R. D. Lillie ◽

P. Pizzolato ◽

C. Reynolds ◽

P. T. Donaldson

Keyword(s):

Mast Cells ◽

Enterochromaffin Cells

Download Full-text

Cisplatin increases the number of enterochromaffin cells containing substance P in rat intestine

Naunyn-Schmiedeberg s Archives of Pharmacology ◽

10.1007/s00210-018-1493-5 ◽

2018 ◽

Vol 391 (8) ◽

pp. 847-858 ◽

Cited By ~ 8

Author(s):

Yusuke Obara ◽

Takuji Machida ◽

Yuho Takano ◽

Saki Shiga ◽

Asami Suzuki ◽

...

Keyword(s):

Substance P ◽

Enterochromaffin Cells ◽

Rat Intestine

Download Full-text