Humans ; Enterochromaffin Cells

Most serotonin is found outside the central nervous system and functions much more than a neurotransmitter. Peripheral serotonin is produced by enterochromaffin cells in the gastrointestinal tract and secreted into blood. Serotonin, as a circulating amine, takes part in numerous biological processes including cardiovascular function, bowel motility, glucose metabolism and skeletal change. Serotonin signaling is regulated by serotonin receptors and serotonin transporters in multiple body organs. The drugs that manipulate the serotonergic system have been developed and used for the treatment of many systemic diseases. The richness of serotonergic modulation in the whole body provide both a pharmacologic opportunity and challenge.
Biological Processes ; Central Nervous System ; Enterochromaffin Cells ; Gastrointestinal Tract ; Glucose ; Neurotransmitter Agents ; Receptors, Serotonin ; Serotonin

Migrating motor complex (MMC) is well characterized by the appearance of gastrointestinal contractions in the interdigestive state. This review article discussed the mechanism of gastrointestinal MMC. Luminal administration of 5-hydroxytryptamine (5-HT) initiates duodenal phase II followed by gastrointestinal phase III with a concomitant increase of plasma motilin release in conscious dogs. Duodenal 5-HT concentration is increased during gastric phase II and phase III. Intravenous infusion of motilin increases luminal 5-HT content and induces gastrointestinal phase III. 5-HT4 antagonists significantly inhibits both of gastric and intestinal phase III, while 5-HT3 antagonists inhibited only gastric phase III. These suggest that gastrointestinal MMC cycle is mediated via the interaction between motilin and 5-HT by the positive feedback mechanism. Gastric MMC is regulated via vagus, 5-HT3/4 receptors and motilin, while intestinal MMC is regulated via intrinsic primary afferent neurons and 5-HT4 receptors. Stress is highly associated with the pathogenesis of functional dyspepsia. Acoustic stress attenuates gastric phase III without affecting intestinal phase III in conscious dogs, via reduced vagal activity and increased sympathetic activity. It has been shown that subset of functional dyspepsia patients show reduced vagal activity and impaired gastric phase III. The physiological importance of gastric MMC is a mechanical and chemical cleansing of the empty stomach in preparation for the next meal. The impaired gastric MMC may aggravate dyspeptic symptoms following a food ingestion. Thus, maintaining gastric MMC in the interdigestive state is an important factor to prevent the postprandial dyspeptic symptoms.
Acoustics ; Animals ; Autonomic Pathways ; Contracts ; Dogs ; Dyspepsia ; Eating ; Enterochromaffin Cells ; Humans ; Infusions, Intravenous ; Meals ; Motilin ; Myoelectric Complex, Migrating ; Neurons, Afferent ; Phenobarbital ; Plasma ; Receptors, Serotonin, 5-HT4 ; Serotonin ; Serotonin 5-HT3 Receptor Antagonists ; Serotonin 5-HT4 Receptor Antagonists ; Stomach

In this study, immunohistochemistry was used to examine the changes in the density of colonic endocrine cells - argyrophil and argentaffin cells, chromogranin A (CGA), serotonin, somatostatin and glucagon-containing cells in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. Ulcerative colitis was induced by the instillation of 10 mg of TNBS into the colonic lumen through the anus. To confirm the inducement of ulcerative colitis, the macroscopic and microscopic scores as well as the colonic myeloperoxidase (MPO) activities were monitored for 8 days after TNBS instillation in the colonic lumens. In addition, the number of argyrophil and argentaffin cells, CGA, serotonin, somatostatin and glucagon-immunoreactive cells were counted in the colonic mucosa, respectively. After TNBS instillation into the lumen of the colon from the anus in rats, increases in macroscopic and microscopic scores in the colon tissues were observed along with increases in the colonic MPO activities. Therefore, ulcerative colitis was relatively well induced by the TNBS instillations. Marked decreases in the number of colonic endocrine cells were detected in the TNBS-treated animal compared to the sham control. These results suggest that colonic endocrine cells were also disrupted by TNBS-induced ulcerative colitis.
Anal Canal ; Animals ; Chromogranin A ; Colitis ; Colitis, Ulcerative ; Colon ; Endocrine Cells ; Enterochromaffin Cells ; Immunohistochemistry ; Mucous Membrane ; Peroxidase ; Rats ; Salicylamides ; Serotonin ; Somatostatin

Carcinoid tumors are derived from enterochromaffin cells that are capable of producing a wide range of neuroendocrine mediators including serotonin or 5-hydroxytryptamine. Carcinoid syndrome occurs when mediators produced by the tumor and normally metabolized by the liver escape into the systemic circulation. The syndrome classically involves the gastrointestinal tract, respiratory system, cardiovascular system and the skin. Flushing is almost universal in the syndrome. A 23-year-old woman came to our hospital presenting with flushing on face and trunk. The patient had experienced flushing for 2 years and it was aggravated by emotional change, stress, exercise, and eating spicy food. The patient also had abdominal pain, diarrhea, weight loss and hepatomegaly. Urinary 5-hydroxyindoleacetic acid was elevated (81.5 mg/day). Abdominal computed tomography scans showed multiple hepatic masses diagnosed as a carcinoid tumor by computed tomography-guided needle biopsy. Physicians should consider carcinoid syndrome when patients present with flushing and systemic symptoms.
Abdominal Pain ; Biopsy, Needle ; Carcinoid Tumor ; Cardiovascular System ; Collodion ; Diarrhea ; Eating ; Enterochromaffin Cells ; Female ; Flushing ; Gastrointestinal Tract ; Hepatomegaly ; Humans ; Liver ; Porphyrins ; Respiratory System ; Serotonin ; Skin ; Skin Manifestations ; United Nations ; Weight Loss ; Young Adult

Proton-pump inhibitors (PPI) have important roles in the management of acid-related disorders, especially gastro-esophageal reflux disease and peptic ulcer disease. They are considered safe, but some side effects, such as oxyntic cell hyperplasia, glandular cysts, hypergastrinemia and fundic gland polyps, are also reported. Long-term PPI administration in Helicobacter pylori (H. pylori) positive subjects promotes a shift from antral to corpus-predominant gastritis. The shift leads to corpus atrophy eventually that is known predisposing factor of gastric adenocarcinoma. It is recommended that patients being considered for long-term PPI therapy should be tested for H. pylori infection. And if present, H. pylori eradication should be preceded to PPI administration. Also, long-term PPI administration can cause enterochromaffin-like cell hyperplasia. Although the underlying mechanism and pathogenesis are not yet fully understood, it is possible that long-term PPI administration can promote the development of gastric carcinoid tumor. Therefore, to minimize the side effects, it should be used in adequate dose for a precise duration.
Adenocarcinoma ; Atrophy ; Carbamates ; Carcinoid Tumor ; Enterochromaffin-like Cells ; Gastritis ; Gastritis, Atrophic ; Gastroesophageal Reflux ; Helicobacter pylori ; Humans ; Hyperplasia ; Organometallic Compounds ; Parietal Cells, Gastric ; Peptic Ulcer ; Polyps

Proton pump inhibitors (PPIs) are widely used over 20 years for management of symptoms due to acid related diseases such as peptic ulcer and reflux esophagitis. Serious adverse events are extremely rare for short-term PPIs use. Recently, as long-term PPIs use increase, diverse reports have been reported on adverse event related with long-term PPIs use. Long-term PPIs use is generally referred as use of PPIs more than 1 year. Secondary hypergastrinemia after long-term PPIs use is associated with development of fundic gland polyps (FGP) and hyperplasia of enterochromaffin-like cell (ECL) that might be concerned with gastric carcinoid tumor. Furthermore, several studies have posed the relationship between the risk of gastric cancer and long-term PPIs use with co-existing H. pylori infection. The present review summarize the recent accumulated evidence on neoplasm associated with secondary hypergastrinemia after long-term PPIs use.
Carcinoid Tumor ; Enterochromaffin-like Cells ; Esophagitis, Peptic ; Gastritis, Atrophic ; Hyperplasia ; Peptic Ulcer ; Polyps ; Proton Pump Inhibitors ; Proton Pumps ; Protons ; Stomach Neoplasms

PURPOSE: Postinfectiously irritable bowel syndrome (PI-IBS) develops in 3-30% of individuals with bacterial gastroenteritis. Recent studies demonstrated increases in inflammatory components in gut mucosa of PI-IBS patients even after complete resolution of infection. We aimed to investigate histological changes in colon and rectum of PI-IBS subjects after long term period of infection. MATERIALS AND METHODS: We recruited PI-IBS subjects who had been diagnosed IBS after complete resolution of enteritis caused by shigellosis outbreak 3 years earlier. We compared unmatched four groups, PI-IBS (n = 4), non PI-IBS (n = 7), D-IBS (n = 7, diarrhea predominant type) and healthy controls (n = 10). All of them underwent colonoscopic biopsy at three areas, including descending colon (DC), sigmoid colon (SC) and rectum, which were assessed for 5-hydroxytryptamine (5-HT)/peptide YY (PYY)-containing enterochromaffin (EC) cell, intraepithelial (IEL) and lamina propria T lymphocyte (CD3), CD8 lymphocytes, mast cells and CD68/calprotectin+ macrophages. RESULTS: All subjects had no structural or gross abnormalities at colonoscopy. In PI-IBS, 5-HT containing EC cells, PYY containing EC cells, IELs, CD3 lymphocytes, CD8 lymphocytes, mast cells, and CD68 + macrophages were increased compared to control (p < 0.05). In D-IBS, PYY containing EC cells, IELs, and CD3 lymphocytes were increased compared to control (p < 0.05). In PI-IBS, 5-HT containing EC cells tended to increase and PYY containing EC cells, CD8 lymphocytes, mast cells, and CD68+ macrophages were increased compared to non PI-IBS (p < 0.05). Calprotectin + marcrophages were decreased in PI-IBS, non PI-IBS and IBS compared to control. CONCLUSION: The immunoendocrine cells were sporadically increased in PI-IBS, non PI-IBS and D-IBS compared with control. Our findings in a very small number of patients suggest that mucosal inflammation may play a role in long-term PI-IBS, and that other sub-groups of IBS and larger scale studies are needed to confirm this observation.
Adult ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; CD8-Positive T-Lymphocytes/cytology ; Case-Control Studies ; Colon, Descending/pathology ; Colon, Sigmoid/pathology ; Colonoscopy ; Dysentery, Bacillary/*complications ; Enterochromaffin Cells/cytology ; Female ; Humans ; Immunohistochemistry ; Intestinal Mucosa/*pathology ; Irritable Bowel Syndrome/metabolism/*pathology ; Macrophages/cytology ; Male ; Mast Cells/cytology ; Peptide YY/metabolism ; Rectum/pathology ; Serotonin/metabolism

This study was performed in order to assess whether acute stress can increase mast cell and enterochromaffin (EC) cell numbers, and proteinase-activated receptor-2 (PAR2) expression in the rat colon. In addition, we aimed to investigate the involvement of corticotrophin-releasing factor in these stress-related alterations. Eighteen adult rats were divided into 3 experimental groups: 1) a saline-pretreated non-stressed group, 2) a saline-pretreated stressed group, and 3) an astressin-pretreated stressed group. The numbers of mast cells, EC cells, and PAR2-positive cells were counted in 6 high power fields. In proximal colonic segments, mast cell numbers of stressed rats tended to be higher than those of non-stressed rats, and their PAR2-positive cell numbers were significantly higher than those of non-stressed rats. In distal colonic segments, mast cell numbers and PAR2-positive cell numbers of stressed rats were significantly higher than those of non-stressed rats. Mast cell and PAR2-positive cell numbers of astressin-pretreated stressed rats were significantly lower than those of saline-pretreated stressed rats. EC cell numbers did not differ among the three experimental groups. Acute stress in rats increases mast cell numbers and mucosal PAR2 expression in the colon. These stress-related alterations seem to be mediated by release of corticotrophin-releasing factor.
Animals ; Colon/*metabolism ; Corticotropin-Releasing Hormone/antagonists & inhibitors/metabolism/pharmacology/*physiology ; Enterochromaffin Cells/cytology ; Male ; Mast Cells/*cytology/immunology/metabolism ; Peptide Fragments/pharmacology ; Rats ; Rats, Wistar ; Receptor, PAR-2/*metabolism ; Restraint, Physical ; *Stress, Physiological

Carcinoid tumors are rare and they arise from the enterochromaffin cells of the gastrointestinal tract. The rectum is the most common site for gastrointestinal carcinoids, and the majority of rectal carcinoids are found incidentally during colonoscopy. As the use of diagnostic colonoscopy has recently become more common, the number of cases with small rectal carcinoids resected by endoscopic resection has increased. However, distinguishing benign from malignant carcinoids is usually imposible based solely on the histology; therefore, evaluation for the local and distant metastases of rectal carcinoids is necessary even after complete endoscopic resection. We have experienced a case of small rectal carcinoid tumor that was endoscopically completely resected and surgical resection was done for the associated lymph node metastases.
Carcinoid Tumor ; Colonoscopy ; Enterochromaffin Cells ; Gastrointestinal Tract ; Lymph Nodes ; Neoplasm Metastasis ; Rectum