Crosstalk between interleukin-6 and corticotropin-releasing factor modulate submucosal plexus activity and colonic secretion

2013 ◽  
Vol 30 ◽  
pp. 115-124 ◽  
Author(s):  
Dervla O’Malley ◽  
John F. Cryan ◽  
Timothy G. Dinan
Keyword(s):  
Interleukin 6 ◽  
Corticotropin Releasing Factor ◽  
Submucosal Plexus ◽  
Colonic Secretion

scholarly journals VIP is involved in peripheral CRF-induced stimulation of propulsive colonic motor function and diarrhea in male rats

2018 ◽  
Vol 314 (5) ◽  
pp. G610-G622 ◽  
Author(s):  
Seiichi Yakabi ◽  
Lixin Wang ◽  
Hiroshi Karasawa ◽  
Pu-Qing Yuan ◽  
Kazuhiko Koike ◽  
...  
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Motor Function ◽  
Terminal Ileum ◽  
Proximal Colon ◽  
Corticotropin Releasing Factor ◽  
Submucosal Plexus ◽  
Myenteric Neurons ◽  
Colonic Motor ◽  
Fos Expression ◽  
Stimulation Of

We investigated whether vasoactive intestinal peptide (VIP) and/or prostaglandins contribute to peripheral corticotropin-releasing factor (CRF)-induced CRF1 receptor-mediated stimulation of colonic motor function and diarrhea in rats. The VIP antagonist, [4Cl-D-Phe6, Leu17]VIP injected intraperitoneally completely prevented CRF (10 µg/kg ip)-induced fecal output and diarrhea occurring within the first hour after injection, whereas pretreatment with the prostaglandins synthesis inhibitor, indomethacin, had no effect. In submucosal plexus neurons, CRF induced significant c-Fos expression most prominently in the terminal ileum compared with duodenum and jejunum, whereas no c-Fos was observed in the proximal colon. c-Fos expression in ileal submucosa was colocalized in 93.4% of VIP-positive neurons and 31.1% of non-VIP-labeled neurons. CRF1 receptor immunoreactivity was found on the VIP neurons. In myenteric neurons, CRF induced only a few c-Fos-positive neurons in the ileum and a robust expression in the proximal colon (17.5 ± 2.4 vs. 0.4 ± 0.3 cells/ganglion in vehicle). The VIP antagonist prevented intraperitoneal CRF-induced c-Fos induction in the ileal submucosal plexus and proximal colon myenteric plexus. At 60 min after injection, CRF decreased VIP levels in the terminal ileum compared with saline (0.8 ± 0.3 vs. 2.5 ± 0.7 ng/g), whereas VIP mRNA level detected by qPCR was not changed. These data indicate that intraperitoneal CRF activates intestinal submucosal VIP neurons most prominently in the ileum and myenteric neurons in the colon. It also implicates VIP signaling as part of underlying mechanisms driving the acute colonic secretomotor response to a peripheral injection of CRF, whereas prostaglandins do not play a role. NEW & NOTEWORTHY Corticotropin-releasing factor (CRF) in the gut plays a physiological role in the stimulation of lower gut secretomotor function induced by stress. We showed that vasoactive intestinal peptide (VIP)-immunoreactive neurons in the ileal submucosal plexus expressed CRF1 receptor and were prominently activated by CRF, unlike colonic submucosal neurons. VIP antagonist abrogated CRF-induced ileal submucosal and colonic myenteric activation along with functional responses (defecation and diarrhea). These data point to VIP signaling in ileum and colon as downstream effectors of CRF.

Stimulation of interleukin-6 production by corticotropin-releasing factor

1992 ◽  
Vol 143 (1) ◽  
pp. 220-227 ◽  
Author(s):  
Sy-Jye Christine Leu ◽  
Vijendra K. Singh
Keyword(s):  
Interleukin 6 ◽  
Corticotropin Releasing Factor ◽  
Stimulation Of

Role for 5-HT and ACh in submucosal reflexes mediating colonic secretion

1995 ◽  
Vol 269 (3) ◽  
pp. G346-G351 ◽  
Author(s):  
M. Sidhu ◽  
H. J. Cooke
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Submucosal Plexus ◽  
Reflex Pathways ◽  
Colonic Secretion ◽  
Serotoninergic Receptors

Neural reflex pathways activated in response to mucosal stroking were investigated in segments of distal colon from guinea pigs. Stroking the mucosal surface of whole thickness or muscle-stripped segments with a brush at 1/s evoked an increase in short-circuit current (Isc) whose duration and amplitude were dependent on the number of strokes. The increase in Isc induced by mucosal stroking was virtually abolished by inhibitors of chloride secretion and by tetrodotoxin. The response was reduced by atropine, renzapride, and N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide but not by mecamylamine, ketanserin, tropisetron, or SDZ-205-557. Mucosal application of 5-hydroxytryptamine and 5-hydroxyindalpine increased Isc, which was attenuated by tetrodotoxin and renzapride. The results suggest that mucosal stroking evokes chloride secretion by activating neural reflex pathways utilizing serotoninergic receptors, of the 5-HT1P class, as well as muscarinic receptors within the submucosal plexus.

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