scholarly journals Role of Substance P in the Pathophysiology of Inflammatory Bowel Disease and Its Correlation With the Degree of Inflammation

Cureus ◽  
2020 ◽  
Author(s):  
Mauli Patel ◽  
Sharathshiva Valaiyaduppu Subas ◽  
Mohammad R Ghani ◽  
Vishal Busa ◽  
Ahmed Dardeir ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Substance P ◽  
Bowel Disease ◽  
Inflammatory Bowel

Role of perivascular nerve and sensory neurotransmitter dysfunction in inflammatory bowel disease

2021 ◽  
Author(s):  
Charles E. Norton ◽  
Elizabeth A. Grunz-Borgmann ◽  
Marcia L. Hart ◽  
Benjamin W. Jones ◽  
Craig L. Franklin ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Blood Flow ◽  
Substance P ◽  
Bowel Disease ◽  
Vascular Dysfunction ◽  
Receptor Expression ◽  
Mesenteric Arteries ◽  
Increased Risk ◽  
Inflammatory Bowel

Inflammatory Bowel Disease (IBD) is associated with both impaired intestinal blood flow and increased risk of cardiovascular disease, but the functional role of perivascular nerves that control vasomotor function of mesenteric arteries (MAs) perfusing the intestine during IBD is unknown. Because perivascular sensory nerves and their transmitters calcitonin gene-related peptide (CGRP) and substance P (SP) are important mediators of both vasodilation and inflammatory responses, our objective was to identify IBD-related deficits in perivascular sensory nerve function and vascular neurotransmitter signaling. In MAs from an IL-10-/- mouse model, IBD significantly impairs electrical field stimulation (EFS)-mediated sensory vasodilation and inhibition of sympathetic vasoconstriction, despite decreased sympathetic nerve density and vasoconstriction. The MA content and EFS-mediated release of both CGRP and SP are decreased with IBD, but IBD has unique effects on each transmitter. CGRP nerve density, receptor expression, hyperpolarization and vasodilation are preserved with IBD. In contrast, SP nerve density and receptor expression are increased, and SP hyperpolarization and vasodilation are impaired with IBD. A key finding is that blockade of SP receptors restores EFS-mediated sensory vasodilation and enhanced CGRP-mediated vasodilation in MAs from IBD but not Control mice. Together, these data suggest that an aberrant role for the perivascular sensory neurotransmitter SP and its downstream signaling in MAs underlies vascular dysfunction with IBD. We propose that with IBD, SP signaling impedes CGRP-mediated sensory vasodilation, contributing to impaired blood flow. Thus, substance P and NK1 receptors may represent an important target for treating vascular dysfunction in IBD.

scholarly journals Changes in the expression of substance P in nerve fibres of the colonic mucosa in dogs suffering from inflammatory bowel disease

2020 ◽  
Vol 68 (2) ◽  
pp. 154-159
Author(s):  
Andrzej Rychlik ◽  
Slawomir Gonkowski ◽  
Krystyna Makowska ◽  
Ewa Kaczmar ◽  
Jaroslaw Calka
Keyword(s):  
Inflammatory Bowel Disease ◽  
Substance P ◽  
Bowel Disease ◽  
Disease Process ◽  
Nerve Fibres ◽  
Mucosal Layer ◽  
Inflammatory Bowel ◽  
Healthy Dogs ◽  
Pain Stimuli

AbstractDue to its difficult diagnosis and complicated treatment, inflammatory bowel disease (IBD) in dogs is a challenge for the veterinarian. Several aspects connected with pathological changes during IBD still remain unknown. Since one of these aspects is the participation of intestinal innervation in the evolution of the disease, the aim of this study was to demonstrate changes in the number and distribution of intramucosal colonic nerve fibres immunoreactive to substance P (SP) arising as the disease progresses. SP is one of the most important neuronal factors in intestinal innervation which, among other tasks, takes part in the conduction of pain stimuli. Using routine immunofluorescence technique, the density of nerve fibres containing SP was evaluated within mucosal biopsy specimens collected from the descending colon of healthy dogs and animals suffering from IBD of varying severity. The results of the study indicate that during severe IBD the number of nerve fibres containing SP located in the colonic mucosal layer increases in comparison to control animals. The number of SP-positive intramucosal nerves amounted to 10.99 ± 2.11 nerves per observation field in healthy dogs, 14.62 ± 2.86 in dogs with mild IBD, 14.80 ± 0.91 in dogs with moderate IBD and 19.03 ± 6.11 in animals with severe IBD. The observed changes were directly proportional to the intensity of the disease process. These observations may suggest a role of this neuronal substance in pathological processes occurring during IBD. Although the exact mechanism of the observed changes has not been completely explained, the results obtained in this investigation may contribute to improving the diagnosis and treatment of this disease, as well as the staging of canine IBD in veterinary practice.

scholarly journals Treatment with Neurokinin-1 Receptor Antagonist Reduces Severity of Inflammatory Bowel Disease Induced by Cryptosporidium parvum

2002 ◽  
Vol 9 (2) ◽  
pp. 333-340 ◽  
Author(s):  
Ioana M. Sonea ◽  
Mitchell V. Palmer ◽  
Dhuha Akili ◽  
James A. Harp
Keyword(s):  
Inflammatory Bowel Disease ◽  
Substance P ◽  
Receptor Antagonist ◽  
Bowel Disease ◽  
Neurokinin 1 Receptor ◽  
Intestinal Lesions ◽  
Inflammatory Bowel ◽  
Neurokinin 1 ◽  
Neurotransmitter Substance

ABSTRACT Inflammatory bowel disease (IBD) is a chronic, debilitating disorder of uncertain and perhaps multiple etiologies. It is believed to be due in part to disregulation of the immune system. Neuroimmune interactions may be involved in induction or maintenance of IBD. In the present study, we examined the potential role of a neurotransmitter, substance P, in a mouse model of IBD. We found that binding sites for substance P, and more specifically, neurokinin-1 receptors, were upregulated in intestinal tissue of mice with IBD-like syndrome. Dosing of mice with LY303870, a neurokinin-1 receptor antagonist, reduced the severity of IBD, and treatment of mice with preexisting IBD allowed partial healing of lesions. We hypothesize that blocking the binding of substance P to the neurokinin-1 receptor interrupts the inflammatory cascade that triggers and maintains intestinal lesions of IBD.

The role of osteopontin (OPN/SSP1) gene variants in inflammatory bowel disease

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
J Glas ◽  
J Seiderer ◽  
HP Török ◽  
B Göke ◽  
T Ochsenkühn ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Gene Variants ◽  
Inflammatory Bowel

Nutrition in inflammatory bowel disease

2009 ◽  
Vol 150 (18) ◽  
pp. 839-845 ◽  
Author(s):  
János Banai
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Fast Food ◽  
Optimal Growth ◽  
Developed Countries ◽  
Aetiological Factor ◽  
Artificial Nutrition ◽  
Food Preservatives ◽  
Inflammatory Bowel

Aetiology of inflammatory bowel disease (IBD) is complex and probably multifactorial. Nutrition has been proposed to be an important aetiological factor for development of IBD. Several components of the diet (such as sugar, fat, fibre, fruit and vegetable, protein, fast food, preservatives etc.) were examined as possible causative agents for IBD. According to some researchers infant feeding (breast feeding) may also contribute to the development of IBD. Though the importance of environmental factors is evidenced by the increasing incidence in developed countries and in migrant population in recent decades, the aetiology of IBD remained unclear. There are many theories, but as yet no dietary approaches have been proved to reduce the risk of developing IBD. The role of nutrition in the management of IBD is better understood. The prevention and correction of malnutrition, the provision of macro- and micronutrients and vitamins and the promotion of optimal growth and development of children are key points of nutritional therapy. In active disease, the effective support of energy and nutrients is a very important part of the therapy. Natural and artificial nutrition or the combination of two can be choosen for supporting therapy of IBD. The author summarises the aetiological and therapeutic role of nutrition in IBD.

scholarly journals Tu1789 – Treatment Response to Ustekinumab and Vedolizumab in Inflammatory Bowel Disease: the Predictive Role of Gut Microbiota

2019 ◽  
Vol 156 (6) ◽  
pp. S-1124
Author(s):  
Clara Caenepeel ◽  
Sara Vieira-Silva ◽  
Jorge F. Vázquez-Castellanos ◽  
Bram Verstockt ◽  
Marc Ferrante ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Treatment Response ◽  
Bowel Disease ◽  
Predictive Role ◽  
Inflammatory Bowel

scholarly journals The role of heme oxygenase and carbon monoxide in inflammatory bowel disease

Redox Report ◽  
2010 ◽  
Vol 15 (5) ◽  
pp. 193-201 ◽  
Author(s):  
Tomohisa Takagi ◽  
Yuji Naito ◽  
Kazuhiko Uchiyama ◽  
Toshikazu Yoshikawa
Keyword(s):  
Inflammatory Bowel Disease ◽  
Carbon Monoxide ◽  
Heme Oxygenase ◽  
Bowel Disease ◽  
Inflammatory Bowel

Ethnic Differences in the Smoking-Related Risk of Inflammatory Bowel Disease: A Systematic Review and Meta-Analysis

2021 ◽  
Author(s):  
Daniele Piovani ◽  
Claudia Pansieri ◽  
Soumya R R Kotha ◽  
Amanda C Piazza ◽  
Celia-Louise Comberg ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Latin American ◽  
Bowel Disease ◽  
Meta Analysis ◽  
Study Data ◽  
Future Research ◽  
Related Risk ◽  
Increased Risk ◽  
Inflammatory Bowel

Abstract Background and aims The association between smoking and inflammatory bowel disease (IBD) relies on old meta-analyses including exclusively non-Jewish White populations. Uncertainty persists regarding the role of smoking in other ethnicities. Methods We systematically searched Medline/PubMed, Embase and Scopus for studies examining tobacco smoking and the risk of developing IBD, i.e., Crohn’s disease (CD) or ulcerative colitis (UC). Two authors independently extracted study data and assessed each study’s risk-of-bias. We examined heterogeneity and small-study effect, and calculated summary estimates using random-effects models. Stratified analyses and meta-regression were employed to study the association between study-level characteristics and effect estimates. The strength of epidemiological evidence was assessed through prespecified criteria. Results We synthesized 57 studies examining the smoking-related risk of developing CD and UC. Non-Jewish White smokers were at increased risk of CD (29 studies; RR: 1.95, 95% CI: 1.69‒2.24; moderate evidence). No association was observed in Asian, Jewish and Latin-American populations (11 studies; RR: 0.97; 95% CI: 0.83–1.13), with no evidence of heterogeneity across these ethnicities. Smokers were at reduced risk of UC (51 studies; RR: 0.55, 95% CI: 0.48–0.64; weak evidence) irrespectively of ethnicity; however, cohort studies, large studies and those recently published showed attenuated associations. Conclusions This meta-analysis did not identify any increased risk of CD in smokers in ethnicities other than non-Jewish Whites, and confirmed the protective effect of smoking on UC occurrence. Future research should characterize the genetic background of CD patients across different ethnicities to improve our understanding on the role of smoking in CD pathogenesis.

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