Mediation of Interleukin‐23 and Tumor Necrosis Factor–Driven Reactive Arthritis by Chlamydia ‐Infected Macrophages in SKG Mice - CNRS - Centre national de la recherche scientifique Accéder directement au contenu
Article Dans Une Revue Arthritis & rheumatology Année : 2021

Mediation of Interleukin‐23 and Tumor Necrosis Factor–Driven Reactive Arthritis by Chlamydia ‐Infected Macrophages in SKG Mice

Charles Armitage
Ranjeny Thomas

Résumé

Pseudomonas aeruginosa (P.a) is one of the most critical antibiotic resistant bacteria in the world and is the most prevalent pathogen in cystic fibrosis (CF), causing chronic lung infections that are considered one of the major causes of mortality in CF patients. Although several studies have contributed to understanding P.a within-host adaptive evolution at a genomic level, it is still difficult to establish direct relationships between the observed mutations, expression of clinically relevant phenotypes, and clinical outcomes. Here, we performed a comparative untargeted LC/HRMS-based metabolomics analysis of sequential isolates from chronically infected CF patients to obtain a functional view of P.a adaptation. Metabolic profiles were integrated with expression of bacterial phenotypes and clinical measurements following multiscale analysis methods. Our results highlighted significant associations between P.a “metabotypes”, expression of antibiotic resistance and virulence phenotypes, and frequency of clinical exacerbations, thus identifying promising biomarkers and therapeutic targets for difficult-to-treat P.a infections

Dates et versions

hal-03839613 , version 1 (04-11-2022)

Identifiants

Citer

Xavier Romand, Xiao Liu, M. Arifur Rahman, Zaied Ahmed Bhuyan, Claire Douillard, et al.. Mediation of Interleukin‐23 and Tumor Necrosis Factor–Driven Reactive Arthritis by Chlamydia ‐Infected Macrophages in SKG Mice. Arthritis & rheumatology, 2021, 73 (7), pp.1200-1210. ⟨10.1002/art.41653⟩. ⟨hal-03839613⟩
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