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Data on the effects of gut bacteria eradication via systemic antibiotics on immune neuropathies are currently lacking. This study therefore assessed the effects of antibiotics-induced gut microbiota alterations on the severity of experimental autoimmune neuritis (EAN), a rat model of Guillain-Barr\u00e9 Syndrome (GBS).\u00a0Myelin P0 peptide 180\u2013199 (P0 180\u2013199)-induced EAN severity was compared between adult Lewis rats (12\u00a0weeks old) that received drinking water with or without antibiotics (colistin, metronidazole, vancomycin) and healthy rats, beginning antibiotics treatment immediately after immunization (day 0), and continuing treatment for 14 consecutive days. Neuropathy severity was assessed via a modified clinical score, and then related to gut microbiota alterations observed after fecal 16S rRNA gene sequencing at baseline and after EAN induction. Effectors of gut mucosal and endoneurial immunity were assessed via immunostaining.\u00a0EAN rats showed increased gut mucosal permeability alongside increased mucosal CD8<jats:sup>+<\/jats:sup> T cells compared to healthy controls. Antibiotics treatment alleviated clinical EAN severity and reduced endoneurial T cell infiltration, decreased gut mucosal CD8<jats:sup>+<\/jats:sup> T cells and increased gut bacteria that may be associated with anti-inflammatory mechanisms, like <jats:italic>Lactobacillus<\/jats:italic> or <jats:italic>Parasutterella<\/jats:italic>.\u00a0Our findings point out a relation between gut mucosal immunity and the pathogenesis of EAN, and indicate that antibiotics-induced intestinal immunomodulation might be a therapeutic approach to alleviate autoimmunity in immune neuropathies. Further studies are warranted to evaluate the clinical transferability of these findings to patients with GBS.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Graphical Abstract<\/jats:title>\n          <\/jats:sec>","DOI":"10.1007\/s11481-024-10119-9","type":"journal-article","created":{"date-parts":[[2024,5,31]],"date-time":"2024-05-31T06:01:53Z","timestamp":1717135313000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Antibiotics-Induced Intestinal Immunomodulation Attenuates Experimental Autoimmune Neuritis (EAN)"],"prefix":"10.1007","volume":"19","author":[{"given":"Alina","family":"Sprenger-Sva\u010dina","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ines","family":"Klein","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin K. 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Sprenger-Sva\u010dina, I. Klein, M.K.R. Sva\u010dina, I. Bobylev, C. Schneider, F. Schweitzer, M. Barham, N. Piekarek, F. Farowski report no disclosures. F. Kohle is supported by the Cologne Clinician Scientist Program (CCSP) \/ Faculty of Medicine \/ University of Cologne, funded by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) (Project No. 413543196). H.C. Lehmann received honoraria for speaking and advisory board engagements or academic research support by Akcea, Alnylam, Biogen, Celgene, CSL Behring, Grifols, Gruenenthal, LFB Pharma, Takeda and UCB. M.J.G.T. Vehreschild received research grants from 3\u00a0M, Astellas Pharma, Biontech, DaVolterra, Evonik, Gilead Sciences, Glycom, Immunic, MaaT Pharma, Merck\/MSD, Organobalance, Seres Therapeutics, Takeda Pharmaceutical as well as speaker fees and\/or consulting fees from Alb Fils Kliniken GmbH, Arderypharm, Astellas Pharma, Basilea, Bio-M\u00e9rieux, DaVolterra, Farmak International Holding GmbH, Ferring, Gilead Sciences, Immunic AG, MaaT Pharma, Merck\/MSD, Pfizer, Roche, Organobalance, SocraTec R&D GmbH.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}}],"article-number":"26"}}