| dc.creator | Kountouras J., Papaefthymiou A., Gavalas E., Polyzos S.A., Boziki M., Kyriakou P., Katsinelos P., Zavos C., Liatsos C., Tzivras D., Tzitiridou-Chatzopoulou M., Dardiotis E., Deretzi G., Vardaka E., Doulberis M. | en |
| dc.date.accessioned | 2023-01-31T08:45:29Z | |
| dc.date.available | 2023-01-31T08:45:29Z | |
| dc.date.issued | 2020 | |
| dc.identifier | 10.1016/j.mehy.2020.110135 | |
| dc.identifier.issn | 03069877 | |
| dc.identifier.uri | http://hdl.handle.net/11615/75313 | |
| dc.description.abstract | Helicobacter pylori infection (Hp-I) has been associated with a wide spectrum of gastrointestinal and extra-digestive manifestations, including neurodegenerative diseases. Contradictory data have been published on Hp-I and multiple sclerosis (MS) association, with studies mainly using serology for Hp-I detection that cannot distinguish between active and past infections. We herein hypothesize that humoral and cellular immune responses induced by active Hp-I, beyond damaging locally the gastric mucosa, they may shape the character of systemic autoimmune responses, contributing to MS pathogenesis. To investigate our hypothesis, active Hp-I has been diagnosed in two small MS Greek cohorts by using primarily gastric mucosa histology. A higher prevalence of active Hp-I was documented in MS patients vs. controls (86.4 vs. 50%, P = 0.002) accompanied by exclusive existence of duodenal ulcer and autoimmune diseases with endoscopic and histological findings of chronic active gastritis for the MS group. Our preliminary data suggested that active Hp-I unlike other studies, may not protect, but contribute to MS and we proposed possible Hp-relating mechanisms involved in MS pathophysiology, that merit further evaluation. © 2020 Elsevier Ltd | en |
| dc.language.iso | en | en |
| dc.source | Medical Hypotheses | en |
| dc.source.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85089229521&doi=10.1016%2fj.mehy.2020.110135&partnerID=40&md5=d05b107258157bbbae1b4923a0b432e3 | |
| dc.subject | Article | en |
| dc.subject | autoimmune disease | en |
| dc.subject | cellular immunity | en |
| dc.subject | chronic gastritis | en |
| dc.subject | cohort analysis | en |
| dc.subject | controlled study | en |
| dc.subject | duodenum ulcer | en |
| dc.subject | gastroscopy | en |
| dc.subject | Helicobacter infection | en |
| dc.subject | human | en |
| dc.subject | human tissue | en |
| dc.subject | humoral immunity | en |
| dc.subject | multiple sclerosis | en |
| dc.subject | pathogenesis | en |
| dc.subject | pilot study | en |
| dc.subject | risk factor | en |
| dc.subject | stomach mucosa lesion | en |
| dc.subject | stomach tissue | en |
| dc.subject | complication | en |
| dc.subject | gastritis | en |
| dc.subject | Helicobacter pylori | en |
| dc.subject | multiple sclerosis | en |
| dc.subject | stomach mucosa | en |
| dc.subject | Gastric Mucosa | en |
| dc.subject | Gastritis | en |
| dc.subject | Helicobacter Infections | en |
| dc.subject | Helicobacter pylori | en |
| dc.subject | Humans | en |
| dc.subject | Multiple Sclerosis | en |
| dc.subject | Risk Factors | en |
| dc.subject | Churchill Livingstone | en |
| dc.title | Helicobacter pylori infection as a potential risk factor for multiple sclerosis | en |
| dc.type | journalArticle | en |