Evidence map›Paper›PMID 38944815›Full record

ArticleInflammatory bowel diseases2024

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

Federica Del Chierico, Letizia Masi, Valentina Petito, Valerio Baldelli, Pierluigi Puca, Roberta Benvenuto, Marco Fidaleo, Ivana Palucci, Loris Riccardo Lopetuso, Maria Emiliana Caristo and 8 more

Abstract read
In one paragraph

Article in Inflammatory bowel diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Federica Del ChiericoImmunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.ORCID 0000-0002-4204-4736
Letizia MasiDepartment of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.
Valentina PetitoDepartment of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.ORCID 0000-0003-4396-1613
Valerio BaldelliImmunology, Rheumatology and Infectious Diseases Research Area, Unit of Human Microbiome, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy.
Pierluigi PucaDepartment of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Roberta BenvenutoDepartment of Pathology, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.
Marco FidaleoDepartment of Biology and Biotechnologies Charles Darwin, Università La Sapienza, Rome, Italy.
Ivana PalucciDepartment of Basic Biotechnological Sciences, Intensive and Perioperative Clinics, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.
Loris Riccardo LopetusoDepartment of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.
Maria Emiliana CaristoCen.Ri.S Policlinico Gemelli UNICATT Rome, Rome, Italy.
Cinzia CarrozzaDepartment of Clinical Biochemistry, Laboratory and Infectious Science, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.
Maria Cristina GiustinianiDepartment of Pathology, Fondazione Policlinico Universitario A.Gemelli IRCCS, Rome, Italy.
Noritaka NakamichiFaculty of Pharmacy, Takasaki University of Health and Welfare, 60 Nakaorui-machi, 370-0033, Takasaki, Gunma, Japan.
Yukio KatoFaculty of Pharmacy, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan.ORCID 0000-0001-8135-5679
Lorenza PutignaniUnit 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 GasbarriniDepartment of Medical and Surgical Science, Digestive Disease Center (CeMAD) Translational Research Laboratories, Fondazione Policlinico Universitario "A. Gemelli" IRCCS, Rome, Italy.ORCID 0000-0003-4863-6924
Giovambattista PaniDepartment of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy.
Franco ScaldaferriDepartment of Medical and Surgical Sciences, UOS Inflammatory Bowel Diseases, Center for Diseases of Digestive System (CeMAD), Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy.

Funding

Italian Ministry of Health GR-2016-02364891
6 · The paper itself

Abstract

backgroundInflammatory 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.

methodsA 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.

resultsOctn1 -/- 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.

conclusionsOur 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.

Indexed as

ColitisDextran SulfateDisease Models, AnimalGastrointestinal MicrobiomeInfliximabMice, Inbred C57BLMice, KnockoutOrganic Cation Transport ProteinsAnimalsDysbiosisGastrointestinal AgentsImmunity, MucosalMiceSeverity of Illness IndexSymportersDextran SulfateGastrointestinal AgentsInfliximabOrganic Cation Transport ProteinsSymportersdextran sodium sulphate colitisgut microbiotaOCTN1

Identifiers

PMID38944815
PMCPMC11630256

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.