Solute Transporter OCTN1/Slc22a4 Affects Disease Severity and Response to Infliximab in Experimental Colitis: Role of Gut Microbiota and Immune Modulation.

OCTN1 dextran sodium sulphate colitis gut microbiota

Journal

Inflammatory bowel diseases
ISSN: 1536-4844
Titre abrégé: Inflamm Bowel Dis
Pays: England
ID NLM: 9508162

Informations de publication

Date de publication:
29 Jun 2024
Historique:
received: 08 06 2023
medline: 30 6 2024
pubmed: 30 6 2024
entrez: 30 6 2024
Statut: aheadofprint

Résumé

Inflammatory bowel diseases are chronic disabling conditions with a complex and multifactorial etiology, still incompletely understood. OCTN1, an organic cation transporter, could have a role in modulating the inflammatory response, and some genetic polymorphisms of this molecule have been associated with increased risk of inflammatory bowel diseases. Until now, limited information exists on its potential in predicting/modulating patient's response to therapies. The aim of this study was to evaluate the role of OCTN1 in modifying gut microbiota and mucosal immunity in response to infliximab therapy in murine colitis. A dextran sodium sulphate model of colitis was used to assess the clinical efficacy of infliximab administered intravenously in ocnt1 gene knockout mice and their C57BL/6 controls. Stool, colon, and mesenteric lymph node samples were collected to evaluate differences in gut microbiota composition, histology, and T cell populations, respectively. Octn1 -/- influences the microbiota profile and is associated with a worse dysbiosis in mice with colitis. Infliximab treatment attenuates colitis-associated dysbiosis, with an increase of bacterial richness and evenness in both strains. In comparison with wild type, octn1-/- mice have milder disease and a higher baseline percentage of Treg, Tmemory, Th2 and Th17 cells. Our data support the murine model to study OCTN1 genetic contribution to inflammatory bowel diseases. This could be the first step towards the recognition of this membrane transporter as a biomarker in inflammatory conditions and a predictor of response to therapies. In this article, we evaluated the role of OCTN1, an organic cation transporter, in modifying gut microbiota and immune T cell populations, as well as its effects on experimental colitis and the response to infliximab treatment.

Sections du résumé

BACKGROUND BACKGROUND
Inflammatory bowel diseases are chronic disabling conditions with a complex and multifactorial etiology, still incompletely understood. OCTN1, an organic cation transporter, could have a role in modulating the inflammatory response, and some genetic polymorphisms of this molecule have been associated with increased risk of inflammatory bowel diseases. Until now, limited information exists on its potential in predicting/modulating patient's response to therapies. The aim of this study was to evaluate the role of OCTN1 in modifying gut microbiota and mucosal immunity in response to infliximab therapy in murine colitis.
METHODS METHODS
A dextran sodium sulphate model of colitis was used to assess the clinical efficacy of infliximab administered intravenously in ocnt1 gene knockout mice and their C57BL/6 controls. Stool, colon, and mesenteric lymph node samples were collected to evaluate differences in gut microbiota composition, histology, and T cell populations, respectively.
RESULTS RESULTS
Octn1 -/- influences the microbiota profile and is associated with a worse dysbiosis in mice with colitis. Infliximab treatment attenuates colitis-associated dysbiosis, with an increase of bacterial richness and evenness in both strains. In comparison with wild type, octn1-/- mice have milder disease and a higher baseline percentage of Treg, Tmemory, Th2 and Th17 cells.
CONCLUSIONS CONCLUSIONS
Our data support the murine model to study OCTN1 genetic contribution to inflammatory bowel diseases. This could be the first step towards the recognition of this membrane transporter as a biomarker in inflammatory conditions and a predictor of response to therapies.
In this article, we evaluated the role of OCTN1, an organic cation transporter, in modifying gut microbiota and immune T cell populations, as well as its effects on experimental colitis and the response to infliximab treatment.

Autres résumés

Type: plain-language-summary (eng)
In this article, we evaluated the role of OCTN1, an organic cation transporter, in modifying gut microbiota and immune T cell populations, as well as its effects on experimental colitis and the response to infliximab treatment.

Identifiants

pubmed: 38944815
pii: 7701819
doi: 10.1093/ibd/izae135
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Italian Ministry of Health
ID : GR-2016-02364891

Informations de copyright

© 2024 Crohn’s & Colitis Foundation. Published by Oxford University Press on behalf of Crohn’s & Colitis Foundation.

Auteurs

Federica Del Chierico (F)

Immunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Letizia Masi (L)

Department of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.

Valentina Petito (V)

Department of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.

Valerio Baldelli (V)

Immunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Pierluigi Puca (P)

Department of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy.

Roberta Benvenuto (R)

Department of Pathology, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.

Marco Fidaleo (M)

Department of Biology and Biotechnologies Charles Darwin, Università La Sapienza, Rome, Italy.

Ivana Palucci (I)

Department of Basic Biotechnological Sciences, Intensive and Perioperative Clinics, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.
Institute of Microbiology, Catholic University of the Sacred Heart, Rome, Italy.

Loris Riccardo Lopetuso (LR)

Department of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Department of Medicine and Ageing Sciences, "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.
Center for Advanced Studies and Technology (CAST), "G. d'Annunzio" University of Chieti-Pescara, Chieti, Italy.

Maria Emiliana Caristo (ME)

Cen.Ri.S Policlinico Gemelli UNICATT Rome, Rome, Italy.

Cinzia Carrozza (C)

Department of Clinical Biochemistry, Laboratory and Infectious Science, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.

Maria Cristina Giustiniani (MC)

Department of Pathology, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.

Noritaka Nakamichi (N)

Faculty of Pharmacy, Takasaki University of Health and Welfare, 60 Nakaorui-machi, 370-0033, Takasaki, Gunma, Japan.

Yukio Kato (Y)

Faculty of Pharmacy, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan.

Lorenza Putignani (L)

Unit of Microbiology and Diagnostic Immunology, Unit of Microbiomics and Immunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.

Antonio Gasbarrini (A)

Department of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.
Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy.
Department of Medical and Surgical Science, Digestive Disease Center (CeMAD), Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.

Giovambattista Pani (G)

Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy.

Franco Scaldaferri (F)

Department of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy.

Classifications MeSH