The Cross-Talk between Microbiome and Metabolome in Rheumatoid Arthritis

Author:

La Barbera Lidia1,Rizzo Chiara1,Grasso Giulia1,Macaluso Federica2,Camarda Federica1,Ciccia Francesco3ORCID,Guggino Giuliana1

Affiliation:

1. Rheumatology Section, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, University of Palermo, Piazza delle Cliniche 2, 90110 Palermo, Italy

2. Rheumatology Unit, Department of Internal Medicine, University of Modena and Reggio Emilia, AUSL-IRCCS, Via Giovanni Amendola, 2, 42122 Reggio Emilia, Italy

3. Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, S. Andrea delle Dame—Via L. De Crecchio 7, 0138 Naples, Italy

Abstract

Modern “omics” sciences, including metabolomics and microbiomics, are currently being applied to inflammatory autoimmune diseases, such as rheumatoid arthritis (RA), to investigate the interplay between microbiota, metabolic function, and the immune system. In recent decades, robust evidence has suggested that disruption of the normal composition of the microbiome, known as dysbiosis, in the gut and mouth of RA patients contributes to immune dysregulation and alterations in the metabolic pathways, shaping the pathogenesis of the disease and playing a central role in the risk and progression of RA. Metabolic pathways can be influenced by various agents such as the surrounding environment, lifestyle, and exposure to microbiota imbalance. In turn, the body’s metabolic homeostasis influences the immune response, making metabolomics helpful not only to understand pathogenesis pathways, but also to improve early disease detection and therapeutic chances. Combined gut microbiome and metabolome studies set out to unravel the interactions between these two entities, providing insights to discover new treatment targets and potential biomarkers to prevent joint damage. The purpose of this review is to summarize the main recent findings that suggest promising new research directions for the pathogenesis of RA.

Publisher

MDPI AG

Subject

Materials Science (miscellaneous)

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