Intestinal Dysbiosis and Rheumatoid Arthritis: A Link between Gut Microbiota and the Pathogenesis of Rheumatoid Arthritis
Table 1
Natural history of rheumatoid arthritis.
Phase of initiation of the disease (interaction between genetic-hormonal-environmental factors)
Preclinical RA
Clinical RA
Genetic and epigenetic factors
Hormonal factors
Environmental factors
Immunological changes
Immunological changes
Shared epitope, PTPN22, STAT4, CTLA4, TRAF1, PADI4, FCRL3, TNFIP3 DNA methylation Dysregulated histone marks
Relationship man : woman 4 : 1 Arthritis is improved in the pregnancy but relapse in the postpartum
Microbiota oral, pulmonary and intestinal Smoking Silica dust Obesity Diet
Inadequate response to peptides Expansion of autoreactive T cells and B cells Expansion of antibody isotype usage and class switching Changes in soluble cytokine and chemokine networks Altered Th17 cells and Th17/regulatory T cell ratios
Upregulation of signalling molecules Immune-mediated tissue inflammation Alterations of autoantibodies, such as glycosylation Cellular expansion
Clinical manifestations
Clinical manifestations
Presence of autoantibodies (RF, ACPAs) Nonspecific symptoms
Arthritis Bone erosions Systemic symptoms
Forms of intervention
Suspension of smoking Avoid exposure to silica Healthy diet Maintaining an adequate weight Modifications of the microbiota?
In research, the early use of rituximab or abatacept Modifications of the microbiota?
Anti-inflammatory Biological and nonbiological disease-modifying drugs Glucocorticoids
