The trimebutine effect on Helicobacter pylori-related gastrointestinal tract and brain disorders: A hypothesis. (March 2021)

• Record Type: Journal Article
• Authors: Boziki, Marina; Grigoriadis, Nikolaos; Papaefthymiou, Apostolis; Doulberis, Michael; Polyzos, Stergios A.; Gavalas, Emmanuel; Deretzi, Georgia; Karafoulidou, Eleni; Kesidou, Evangelia; Taloumtzis, Charilaos; Theotokis, Paschalis; Sofou, Electra; Katsinelos, Panagiotis; Vardaka, Elisabeth; Fludaras, Ioannis; Touloumtzi, Maria; Koukoufiki, Argiro; Simeonidou, Constantina; Liatsos, Christos; Kountouras, Jannis
• Is Part Of: Neurochemistry international. Volume 144(2021)
• Publication Date: 2021-03
• Subjects: Neurodegeneration -- Neuroinflammation -- Dysbiosis -- Gut-brain axis -- Trimebutine -- Helicobacter pylori; GIT Gastrointestinal tract -- MB Microbiota -- MetS Metabolic syndrome -- IBD Inflammatory bowel disease -- AD Alzheimer's disease -- MS Multiple sclerosis -- BBB Blood-brain barrier -- CNS Central nervous system -- Hp-I Helicobacter pylori infection -- OAG Open–angle glaucoma -- MCI Mild cognitive impairment -- CIS Clinically isolated syndrome -- HE Hepatic encephalopathy -- TM Trimebutine maleate -- GBA Gut-brain axis -- GERD Gastroesophageal reflux disease -- IBS Irritable bowel syndrome -- GIBO Gastrointestinal bacterial overgrowth -- PD Parkinson's disease -- ALS Amyotrophic lateral sclerosis -- NMO Neuromyelitis optica -- ENS Enteric nervous system -- EAE Experimental autoimmune encephalomyelitis -- TNF Tumor necrosis factor -- IL Interleukin -- LPS Lipopolysaccharides -- IFN Interferon -- Aβ42 Amyloid beta 42 -- Gal-3 Galectin-3 -- Hsp Heat shock protein -- IgG Imunoglobulin G -- Hp-NAP Hp neutrophil-activating protein -- FD Functional dyspepsia -- AE Adverse events -- HMGB1 High mobility group box 1 -- RAGE Receptor for advanced glycation end-products -- L-dopa 3, 4-dihydroxyphenylalanine -- DMBT1 Malignant brain tumour 1; Neurochemistry -- Periodicals; Neurochemistry -- Periodicals; Neurochimie -- Périodiques; Neurochemistry; Periodicals; 612.804205
• DOI: 10.1016/j.neuint.2020.104938
• Languages: English
• ISSNs: 0197-0186

Abstract

Abstract: The localization of bacterial components and/or metabolites in the central nervous system may elicit neuroinflammation and/or neurodegeneration. Helicobacter pylori (a non-commensal symbiotic gastrointestinal pathogen) infection and its related metabolic syndrome have been implicated in the pathogenesis of gastrointestinal tract and central nervous system disorders, thus medications affecting the nervous system - gastrointestinal tract may shape the potential of Helicobacter pylori infection to trigger these pathologies. Helicobacter pylori associated metabolic syndrome, by impairing gut motility and promoting bacterial overgrowth and translocation, might lead to brain pathologies. Trimebutine maleate is a prokinetic drug that hastens gastric emptying, by inducing the release of gastrointestinal agents such as motilin and gastrin. Likewise, it appears to protect against inflammatory signal pathways, involved in inflammatory disorders including brain pathologies. Trimebutine maleate also acts as an antimicrobial agent and exerts opioid agonist effect. This study aimed to investigate a hypothesis regarding the recent advances in exploring the potential role of gastrointestinal tract microbiota dysbiosis-related metabolic syndrome and Helicobacter pylori in the pathogenesis of gastrointestinal tract and brain diseases. We hereby proposed a possible neuroprotective role for trimebutine maleate by altering the dynamics of the gut-brain axis interaction, thus suggesting an additional effect of trimebutine maleate on Helicobacter pylori eradication regimens against these pathologies. Highlights: TM may act as a possible antimicrobial agent against bacteria. TM may elicit a benefit towards CNS disease via the vagus nerve. TM may conquer Hp-induced GIT dysmotility and MetS implicated in neurodegeneration. TM may enable "neuroprotective" and/or "anti-inflammatory" microflora establishment. TM may exert a neuroprotective effect as an opioid receptor agonist in the CNS.