Antibiotics-Induced Intestinal Immunomodulation Attenuates Experimental Autoimmune Neuritis (EAN).


Journal

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
ISSN: 1557-1904
Titre abrégé: J Neuroimmune Pharmacol
Pays: United States
ID NLM: 101256586

Informations de publication

Date de publication:
31 May 2024
Historique:
received: 30 11 2023
accepted: 21 04 2024
medline: 31 5 2024
pubmed: 31 5 2024
entrez: 31 5 2024
Statut: epublish

Résumé

The composition of gut microbiota plays a pivotal role in priming the immune system and thus impacts autoimmune diseases. 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-Barré Syndrome (GBS). Myelin P0 peptide 180-199 (P0 180-199)-induced EAN severity was compared between adult Lewis rats (12 weeks 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. EAN rats showed increased gut mucosal permeability alongside increased mucosal CD8

Sections du résumé

BACKGROUND BACKGROUND
The composition of gut microbiota plays a pivotal role in priming the immune system and thus impacts autoimmune diseases. 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-Barré Syndrome (GBS). Myelin P0 peptide 180-199 (P0 180-199)-induced EAN severity was compared between adult Lewis rats (12 weeks 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. EAN rats showed increased gut mucosal permeability alongside increased mucosal CD8

Identifiants

pubmed: 38819756
doi: 10.1007/s11481-024-10119-9
pii: 10.1007/s11481-024-10119-9
doi:

Substances chimiques

Anti-Bacterial Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

26

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Alina Sprenger-Svačina (A)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany. alina.sprenger-svacina@uk-koeln.de.

Ines Klein (I)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Martin K R Svačina (MKR)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Ilja Bobylev (I)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Felix Kohle (F)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Christian Schneider (C)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Department of Neurology, St. Katharinen-Hospital, Frechen, Germany.

Finja Schweitzer (F)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Nadin Piekarek (N)

Experimental Medicine, Faculty of Medicine, University Hospital of Cologne, University of Cologne, Cologne, Germany.

Mohammed Barham (M)

Department II of Anatomy, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.

Maria J G T Vehreschild (MJGT)

Department I of Internal Medicine, Faculty of Medicine and University Hospital of Cologne, Cologne, Germany.
Department of Internal Medicine II, Infectious Diseases, Goethe University, University Hospital Frankfurt, Frankfurt Am Main, Germany.
German Centre for Infection Research (DZIF), partner site Bonn-Cologne, Brunswick, Germany.

Helmar C Lehmann (HC)

Department of Neurology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany.
Department of Neurology, Klinikum Leverkusen gGmbH, Leverkusen, Germany.

Fedja Farowski (F)

Department I of Internal Medicine, Faculty of Medicine and University Hospital of Cologne, Cologne, Germany.
Department of Internal Medicine II, Infectious Diseases, Goethe University, University Hospital Frankfurt, Frankfurt Am Main, Germany.
German Centre for Infection Research (DZIF), partner site Bonn-Cologne, Brunswick, Germany.

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