Faculty Opinions recommendation of Upregulation of intestinal mucosal mast cells expressing VPAC1 in close proximity to vasoactive intestinal polypeptide in inflammatory bowel disease and murine colitis.

Author(s):  
Jonathan Kaunitz
Animals ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1759
Author(s):  
Andrzej Rychlik ◽  
Sławomir Gonkowski ◽  
Jarosław Całka ◽  
Krystyna Makowska

Canine inflammatory bowel disease (IBD) is a group of enteropathies with nonspecific chronic symptoms and poorly understood etiology. Many aspects connected with IBD are not understood. One of them is the participation of the intestinal nervous system in the development of pathological processes. Thus, this study aimed to demonstrate changes in the density of intramucosal nerve fibers containing vasoactive intestinal polypeptide (VIP)—one of the most important intestinal nervous factors caused by the various stages of IBD development. Mucosal biopsy specimens collected from the duodenum, jejunum and descending colon of healthy dogs and dogs with varied severity of IBD were included in the experiment. The density of VIP-like immunoreactive (VIP-LI) nerves was determined by a single immunofluorescence technique and a semi-quantitative method consisting in VIP-LI fiber counts in the field of view (0.1 mm2). The obtained results indicate that IBD induces changes in the density of mucosal VIP-LI nerve fibers in the canine gastrointestinal tract. The initial decrease is followed by an increase in VIP-like immunoreactivity in successive stages of the disease. These observations show that VIP is a neuronal factor that participates in the pathological processes connected with canine IBD. The observed changes probably result from the neuroprotective and/or adaptive properties of VIP. Protective and adaptive reactions induced by inflammation aim to protect the GI tract against damage by proinflammatory factors and ensure the homeostasis in the enteric nervous system (ENS) under the conditions changed by the disease process.


2005 ◽  
Vol 48 (3-4) ◽  
pp. 163-164 ◽  
Author(s):  
Bilge Tunc ◽  
Levent Filik ◽  
Engin Altıntas ◽  
Nesrin Turhan ◽  
Aysel Ulker ◽  
...  

Even though exciting progresses have been until now, further studies are necessary to clearly understand the significance of MMC. Mast cells are thought to participate in the pathogenesis of inflammatory bowel disease and irritable bowel syndrome. However, their role in the pathogenesis remains unsettled. The specific aims of this study were to (1) examine mucosal mast cell counts in the cecum in patient with IBS, and IBD (2) compare MMC between the disease groups. We showed increased MMC count in IBS.


2007 ◽  
Vol 22 (12) ◽  
pp. 2338-2343 ◽  
Author(s):  
Ashkan Farhadi ◽  
Ali Keshavarzian ◽  
Jeremy Z Fields ◽  
Shriram Jakate ◽  
Maliha Shaikh ◽  
...  

1996 ◽  
Vol 28 (1) ◽  
pp. 1-13 ◽  
Author(s):  
S.C. BISCHOFF ◽  
J. WEDEMEYER ◽  
A. HERRMANN ◽  
P.N. MEIER ◽  
C. TRAUTWEIN ◽  
...  

1990 ◽  
Vol 4 (7) ◽  
pp. 285-288
Author(s):  
EY Bissonnette ◽  
RC Benyon ◽  
AD Befus

The etiology and pathogenesis of inflammatory bowel disease (IBD) is poorly understood. However, numerous studies have demonstrated that immunological and inflammatory responses are activated during this disease. A better understanding of these events will help identify appropriate therapeutic interventions. Mast cell hyperplasia is a prominent feature of inflamed intestinal tissue in IBD. Intestinal mast cells are heterogeneous and at least two populations are present in the human intestine. The authors' objective is to explore mast cell properties, activation and mediators that are involved in the induction, maintenance and perpetuation of inflammatory lesions in the intestine. Although some therapies used in IBD can modulate mast cell activities, whether these actions are important in the beneficial effects of the drugs is unknown. Future drug development targeted to the inhibition of mast cells might be of therapeutic value. However, a cascade of different cellular events are involved in IBD development. The complexity of the disease raises difficulties in the development of therapies. Multiple drugs, selective for different phases of the disease or acting on different cells, might be most appropriate, rather than a single, all-encompassing therapeutic agent.


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