Abstract
Simple SummaryCanine inflammatory bowel disease (IBD)—a group of gastrointestinal disorders—is a serious problem in veterinary medicine. The etiology of IBD remains unknown, and its diagnosis and effective treatment are difficult. One of the less-known aspects of IBD pathology is the influence of this disease on the enteric nervous system, which is located in the intestinal wall and regulates most of the gastrointestinal functions. Therefore, the aim of the present study was to evaluate the influence of IBD on the intramucosal nerve fibers containing vasoactive intestinal polypeptide (VIP). VIP is one of the most important substances produced by the enteric nervous structures that is involved in many regulatory processes in the gastrointestinal tract. The obtained results show that IBD induces changes in the density of intramucosal VIP-positive nerve fibers in the canine gastrointestinal tract. It suggests that VIP is involved in the pathological processes occurring during this disease. Observed changes may be a result of neuroprotective and/or adaptive processes regulated by VIP, aimed at the homeostasis maintenance in the inflamed gastrointestinal (GI) tract and induced by proinflammatory factors.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.
Highlights
Canine inflammatory bowel disease (IBD) is a group of idiopathic and inflammatory enteropathies characterized by persistent or recurring gastrointestinal symptoms
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
In dogs suffering from IBD included in the study, a close correlation between symptoms
Summary
Canine inflammatory bowel disease (IBD) is a group of idiopathic and inflammatory enteropathies characterized by persistent or recurring gastrointestinal symptoms. Since knowledge concerning IBD is rather scarce, this disease is a serious problem in modern veterinary. The main clinical symptoms of IBD are vomiting, diarrhea, weight loss, bloating, abdominal cramping and loss of appetite [5]. Clinical symptoms are accompanied by histopathological changes in the small intestine and/or the colon. Recent studies have shown that substances acting as neurotransmitters and/or neuromodulators in the enteric nervous system (ENS) and extrinsic innervation of the gastrointestinal tract could be implicated in the pathogenesis of intestinal inflammations [6,7,8]. The exact roles of the majority of active neuronal substances in the pathophysiology of IBD have not been yet elucidated
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