Differential changes in Substance P, VIP as well as neprilysin levels in patients with gastritis or ulcer

Erin, Nuray; Türker, Sema; Elpek, Özlem; Yıldırım, Bülent

doi:10.1016/j.peptides.2012.03.018

Cited by 21 publications

(19 citation statements)

References 59 publications

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“…Such a protective effect of PANs has been demonstrated in human chronic gastritis by using low doses of capsaicin (64). In patients with gastritis, the neuronal SP level decreased in normally appearing mucosa, whereas nonneuronal SP increased in the diseased area in gastritis and ulcer patients (65), with Helicobactor pylori infection further decreasing neuronal SP levels. The decrease in SP, a gastroprotective factor, appears to predispose patients to mucosal cellular damage in cases of gastritis.…”

Section: Roles Of Tks In Gastritis and Gastric Cancersmentioning

confidence: 89%

Tachykinin: recent developments and novel roles in health and disease

Onaga

2014

Biomolecular Concepts

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Over 80 years has passed since the discovery of substance P (SP), and a variety of peptides of the tachykinin (TK) family have been found and investigated. SP, neurokinin A (NKA), and neurokinin B (NKB) are representative peptides in mammalian species. SP and NKA are major excitatory neurotransmitters in the peripheral nervous system, while NKB is primarily involved in the central nervous system (CNS). Moreover, TK peptides play roles not only as neurotransmitters but also as local factors and are involved in almost all aspects of the regulation of physiological functions and pathophysiological processes. The role of SP as a mediator of pain processing and inflammation in peripheral tissues in coordination with transient receptor potential channels is well established, while novel aspects of TKs in relation to hematopoiesis, venous thromboembolism, tendinopathy, and taste perception have been clarified. In the CNS, the NKB signaling system in the hypothalamus has been shown to play a crucial role in the regulation of gonadotropin hormone secretion and the onset of puberty, and molecular biological studies have elucidated novel prophylaxic activities of TKs against neurogenic movement disorders based on their molecular structure. This review provides an overview of the novel aspects of TKs reported around the world in the last 5 years, with particular focus on nociception, inflammation, hemopoiesis, gonadotropin secretion, and CNS diseases.

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Section: Roles Of Tks In Gastritis and Gastric Cancersmentioning

confidence: 89%

Tachykinin: recent developments and novel roles in health and disease

Onaga

2014

Biomolecular Concepts

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“…In the present study, it was observed that administration of 100 mg/kg insect tea significantly decreased serum levels of SP, MOT and ET-1 in gastric ulcer mice. SP stimulates gastric juice secretion (28) and decreases gastric contractions (29), resulting in delayed gastric emptying and aggravating gastric ulcers in patients with gastritis (30,31). MOT is a powerful inducer of gastrointestinal motor activity (32) and intestinal contractilities, and stimulates the secretion of human gastric pepsin (33,34).…”

Section: Discussionmentioning

confidence: 99%

Insect tea attenuates hydrochloric acid and ethanol‑induced mice acute gastric injury

Cheng

Qian

et al. 2017

Exp Ther Med

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Abstract. The aim of the present study was to investigate the protective effect of insect tea on HCl/ethanol-induced gastric ulcers in ICR mice. The serum levels of vasoactive intestinal peptide, substance P, somatostatin, motilin and endothelin-1 in mice were assessed using commercial kits and gastric tissues of superoxide dismutase (SOD, nitric oxide (NO) and malondialdehyde (MDA) were determined using western blot analysis Insect tea significantly reduced HCl/ethanol-induced gastric juice secretion and increased the pH of gastric juice (P<0.05). Insect tea treatment signfiicantly increased vasoactive intestinal peptide and somatostatin, and significantly decreased motilin, substance P and endothelin levels in the serum (P<0.05). Treatment with insect tea was demonstrated to significantly increase levels of gastric SOD and NO and to reduce levels of MDA in the gastric ulcer mouse model (P<0.05). The gastric expression of inhibitor of nuclear factor-κB (NF-κB), epidermal growth factor (EGF), EGF receptor, neuronal nitric oxide synthase (nNOS), endothelial NOS, Mn-SOD, Cu/Zn-SOD and catalase was significantly increased in mice treated with inset tea compared with untreated model mice (P<0.05). Levels of NF-κB, and inducible NOS were demonstrated to be decreased in mice treated with insect tea compared with untreated model mice (P<0.05). The results of the present study suggest that insect tea has a protective effect against HCl/ethanol-induced gastric ulcers in ICR mice. This effect may be achieved via modulating serum neuropeptide levels, reducing gastric juice secretion, and modulating the inflammation-and antioxidant-associated protein expressions in gastric tissue.

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“…The pathophysiological interactions between H. pylori and the brain-gut axis likely involve ( Figure 1): (1) axon injury or stimulation (neuroinflammation) by bacterial cytotoxins (VacA) [60,72,78] , neutrophil-attractant chemokine IL-8 [79] , and/or neutrophil-activating protein (H. pylori-NAP) [75,79] ; (2) axon damage or stimulation by autoimmunological reactions due to mimicry of VacA, bacterial aquaporin (AQP), H. pylori-NAP and human antigens [51,53,79,80] ; (3) H. pylori-induced production of free radicals [80][81][82] , cytotoxins and cytokines [57][58][59][60][61]78] , which may also result in blood-brain barrier disruption; (4) changes in neurotransmitter secretion in gastric mucosa and spinal cord [56,72,75,81,[83][84][85] ; (5) neuron injury resulting from gastric mucosa atrophy and a decrease in vitamin B12 absorption [86] ; and (6) changes in stomach and intestinal microbiota [6,[87][88][89] .…”

Section: Role Of the Brain-gut Axis In Acute H Pylori Infectionmentioning

confidence: 99%

“…Neuronal and non-neuronal levels of SP, VIP, CGRP and neprilysin activity were examined in freshly frozen biopsies taken from patients with chronic gastritis or ulcers in a study by Erin et al [85] showing that neuronal SP, mucosal VIP and neprilysin levels decreased significantly in normal appearing mucosa in patients with gastritis, while levels of mucosal SP increased in areas of gastritis and ulcer. In this study the presence of H. pylori was associated with further decreases in SP levels.…”

Section: Role Of the Brain-gut Axis In Chronic H Pylori Infectionmentioning

confidence: 99%

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

Budzyński¹

2014

WJG

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Helicobacter pylori (H. pylori) infection is the main pathogenic factor for upper digestive tract organic diseases. In addition to direct cytotoxic and proinflammatory effects, H. pylori infection may also induce abnormalities indirectly by affecting the brain-gut axis, similar to other microorganisms present in the alimentary tract. The brain-gut axis integrates the central, peripheral, enteric and autonomic nervous systems, as well as the endocrine and immunological systems, with gastrointestinal functions and environmental stimuli, including gastric and intestinal microbiota. The bidirectional relationship between H. pylori infection and the brain-gut axis influences both the contagion process and the host's neuroendocrine-immunological reaction to it, resulting in alterations in cognitive functions, food intake and appetite, immunological response, and modification of symptom sensitivity thresholds. Furthermore, disturbances in the upper and lower digestive tract permeability, motility and secretion can occur, mainly as a form of irritable bowel syndrome. Many of these abnormalities disappear following H. pylori eradication. H. pylori may have direct neurotoxic effects that lead to alteration of the brain-gut axis through the activation of neurogenic inflammatory processes, or by microelement deficiency secondary to functional and morphological changes in the digestive tract. In digestive tissue, H. pylori can alter signaling in the brain-gut axis by mast cells, the main brain-gut axis effector, as H. pylori infection is associated with decreased mast cell infiltration in the digestive tract. Nevertheless, unequivocal data concerning the direct and immediate effect of H. pylori infection on the brain-gut axis are still lacking. Therefore, further studies evaluating the clinical importance of these host-bacteria interactions will improve our understanding of H. pylori infection pathophysiology and suggest new therapeutic approaches.

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Differential changes in Substance P, VIP as well as neprilysin levels in patients with gastritis or ulcer

Cited by 21 publications

References 59 publications

Tachykinin: recent developments and novel roles in health and disease

Tachykinin: recent developments and novel roles in health and disease

Insect tea attenuates hydrochloric acid and ethanol‑induced mice acute gastric injury

Brain-gut axis in the pathogenesis ofHelicobacter pyloriinfection

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