Calcitonin Gene-Related Peptide Is a Promising Marker in Ulcerative Colitis

Li, Fujun; Zou, Yiyou; Cui, Yi; Yin, Yani; Guo, G. B.; Lu, Fanggen

doi:10.1007/s10620-012-2406-y

Cited by 21 publications

(14 citation statements)

References 30 publications

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“…Similarly, CGRP is involved in the regulation of cytokines secretion and leads to a decrease in the level of TNF-α and IL-1β [60]. Upregulated expression of CGRP was noted during numerous pathological states in the GI tract, including peptic ulcers, chemically induced inflammation of porcine descending colon, and ulcerative colitis [61][62][63]. Additionally, as a sensory neuropeptide, it is unquestionably involved in the conduction of pain accompanying the inflammation [28].…”

Section: Discussionmentioning

confidence: 99%

Influence of Acrylamide Administration on the Neurochemical Characteristics of Enteric Nervous System (ENS) Neurons in the Porcine Duodenum

Palus¹,

Całka²

2019

IJMS

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The digestive tract, especially the small intestine, is one of the main routes of acrylamide absorption and is therefore highly exposed to the toxic effect of acrylamide contained in food. The aim of this experiment was to elucidate the effect of low (tolerable daily intake—TDI) and high (ten times higher than TDI) doses of acrylamide on the neurochemical phenotype of duodenal enteric nervous system (ENS) neurons using the pig as an animal model. The experiment was performed on 15 immature gilts of the Danish Landrace assigned to three experimental groups: control (C) group—pigs administered empty gelatine capsules, low dose (LD) group—pigs administered capsules with acrylamide at the TDI dose (0.5 μg/kg body weight (b.w.)/day), and the high dose (HD) group—pigs administered capsules with acrylamide at a ten times higher dose than the TDI (5 μg/kg b.w./day) with a morning feeding for 4 weeks. Administration of acrylamide, even in a low (TDI) dose, led to an increase in the percentage of enteric neurons immunoreactive to substance P (SP), calcitonin gene-related peptide (CGRP), galanin (GAL), neuronal nitric oxide synthase (nNOS), and vesicular acetylcholine transporter (VACHT) in the porcine duodenum. The severity of the changes clearly depended on the dose of acrylamide and the examined plexus. The obtained results suggest the participation of these neuroactive substances in acrylamide-inducted plasticity and the protection of ENS neurons, which may be an important line of defence from the harmful action of acrylamide.

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Section: Discussionmentioning

confidence: 99%

Influence of Acrylamide Administration on the Neurochemical Characteristics of Enteric Nervous System (ENS) Neurons in the Porcine Duodenum

Palus¹,

Całka²

2019

IJMS

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“…CGRP in particular has been the focus of many studies trying to unveil its involvement in a range of inflammatory models and immune conditions e.g., diabetes (Morrison et al, 2009), sepsis (De Winter et al, 2009), EAE (Mikami et al, 2012a) Crohn's Disease (Smith and Smid, 2005), and ulcerative colitis (Engel et al, 2012; Li et al, 2013a). In rats, dextran sulfate sodium (DSS)-induced colitis worsened when treated with a CGRP antagonist suggesting a protective role for CGRP in colitis (Engel et al, 2010).…”

Section: Cgrp and Immunitymentioning

confidence: 99%

Calcitonin gene-related peptide is a key neurotransmitter in the neuro-immune axis

2014

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The question of how the neural and immune systems interact in host defense is important, integrating a system that senses the whole body with one that protects. Understanding the mechanisms and routes of control could produce novel and powerful ways of promoting and enhancing normal functions as well as preventing or treating abnormal functions. Fragmentation of biological research into specialities has resulted in some failures in recognizing and understanding interactions across different systems and this is most striking across immunology, hematology, and neuroscience. This reductionist approach does not allow understanding of the in vivo orchestrated response generated through integration of all systems. However, many factors make the understanding of multisystem cross-talk in response to a threat difficult, for instance the nervous and immune systems share communication molecules and receptors for a wide range of physiological signals. But, it is clear that physical, hard-wired connections exist between the two systems, with the key link involving sensory, unmyelinated nerve fibers (c fibers) containing the neuropeptide calcitonin gene-related peptide (CGRP), and modified macrophages, mast cells and other immune and host defense cells in various locations throughout the body. In this review we will therefore focus on the induction of CGRP and its key role in the neuroimmune axis.

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“…In contrast to SP, CGRP is anti-inflammatory in many tissues 50,51 and participates in immune responses by decreasing the release of proinflammatory cytokines from multiple cell types 52,53 . In patients with IBD, CGRP is decreased in the intestinal mucosa, and the magnitude of this decrease is correlated with the severity of IBD symptoms 54 . CGRP knockout mice are susceptible to colitis 44 , further implicating an important protective role for CGRP in IBD.…”

Section: Discussionmentioning

confidence: 99%

Altered substance P signaling underlies perivascular sensory nerve dysfunction in inflammatory bowel disease

Norton

Grunz-Borgmann

Hart

et al. 2020

Preprint

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Objective: Inflammatory Bowel Disease (IBD) is associated with cardiovascular disease risk and impaired intestinal blood flow, but the functional role of perivascular nerves that control vasomotor function of mesenteric arteries (MAs) perfusing the intestine is unknown in IBD. 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.Approach and Results: In MAs from an IL-10 -/mouse model, we found that IBD significantly impairs EFS-mediated sensory vasodilation and sensory inhibition of sympathetic vasoconstriction, despite decreased sympathetic nerve density and vasoconstriction. The MA content and EFS-mediated release of both CGRP and SP are slightly decreased with IBD, but IBD has different 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 critical finding is that blocking neurokinin 1 (SP) receptors restored EFS-mediated sensory vasodilation and enhanced CGRP-mediated vasodilation in MAs from IBD but not Control mice.Conclusions: An aberrant role for the perivascular sensory neurotransmitter SP and its downstream signaling in MAs underlies vascular dysfunction with IBD. With IBD, SP signaling impedes CGRP-mediated sensory vasodilation, contributing to impaired blood flow. Substance P and NK1 receptors may represent an important target for treating vascular dysfunction in IBD.

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Calcitonin Gene-Related Peptide Is a Promising Marker in Ulcerative Colitis

Abstract: Levels of CGRP protein and mRNA expression in the colonic mucosa of patients are closely associated with UC severity and corroborate traditional indices used to assess the disease.

Cited by 21 publications

References 30 publications

Influence of Acrylamide Administration on the Neurochemical Characteristics of Enteric Nervous System (ENS) Neurons in the Porcine Duodenum

Influence of Acrylamide Administration on the Neurochemical Characteristics of Enteric Nervous System (ENS) Neurons in the Porcine Duodenum

Calcitonin gene-related peptide is a key neurotransmitter in the neuro-immune axis

Altered substance P signaling underlies perivascular sensory nerve dysfunction in inflammatory bowel disease

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