Expansion of Rare and Harmful Lineages is Associated with Established Rheumatoid Arthritis

Abstract

Objectives: To characterize the gut microbiota profile in rheumatoid arthritis (RA) patients and investigate its association with certain characteristics of RA. Patients and methods: A nested case–control cohort of 40 patients with RA and 40 sex-age matched controls was studied. Subjects with diabetes, with any other inflammatory disease, practicing extreme diets, taking antibiotics, probiotics or under any new treatment for at least three months prior to sampling were excluded. The microbiota composition was determined by 16S rRNA pyrosequencing and bioinformatics analysis by Quantitative Insights Into Microbial Ecology (QIIME). Other variables included clinical-laboratory variables and average Disease Activity Score 28 points during the follow-up period. Multiple linear regression models were constructed to investigate the possible risk factors for the microbiota. Results: β-diversity data showed that patients tend to differ from healthy subjects according to their microbiota (p = 0.07). The analysis showed an increase in Collinsella aerofaciens, Sedimentibacter and Enterococcus genera in patients compared to controls, as well as a decrease in Dorea formicigenerans. Likewise, an increase in the activity of arginine deiminase was observed, which was found in approximately 90% of the RA genes of the genus Collinsela. The sequence number of Collinsella aerofaciens was independently associated with age (B (95%CI), −0.347 (−21.6, −2.1)), high ACPA (0.323 (27.4–390.0)) and smoking (0.300 (8.8–256.4)) in RA patients. In addition, we observed decreases in Sarcina, 02d06 and Porphyromonas bacterial lineages. Conclusion: Patients with RA present dysbiosis, resulting from an abundance of certain bacterial lineages and a decrease in others. These alterations could influence the maintenance of autoimmunity to this disease.

Differential Microbial Pattern Description in Subjects with Autoimmune-Based Thyroid Diseases: A Pilot Study

“…Gut microbiota is a promising agent for the development of personalized medicine as it collects information about its host, like diet or environmental factors [ 8 ]. Recent evidence suggest that the alteration of gut microbiota may have connection with autoimmune diseases [ 9 , 10 , 11 , 12 ].…”

The Role of Nutritional Factors and Intestinal Microbiota in Rheumatoid Arthritis Development

“…The subsequent findings have not been completely consistent across the literature, but a repeated feature has been the increase of Prevotella species in early RA [ 47 , 48 , 49 , 50 ], associated to a relative decrease in the Bacteroides genus [ 48 , 51 ]. The overrepresentation of Prevotella species is usually no longer found in established and treated RA patients [ 52 , 53 , 54 ]. In particular, Prevotella copri raised researcher’s interest, because of worsening arthritis when transferred in mice models [ 47 , 48 ].…”

“…Nevertheless, additional immunological studies on human samples (blood, stool, or gut biopsies) are necessary to clarify the mechanism linking P. copri to the onset of RA. Finally, other bacterial species have been associated with human RA, such as Collinsella aerofaciens [ 53 , 54 ]. The latter also worsens arthritis in mice models [ 53 , 54 ], which underlines the fact that there may not be a single bacterial culprit, but probably a complex interplay between several microorganisms and host defenses.…”

“…Finally, other bacterial species have been associated with human RA, such as Collinsella aerofaciens [53,54]. The latter also worsens arthritis in mice models [53,54], which underlines the fact that there may not be a single bacterial culprit, but probably a complex interplay between several microorganisms and host defenses.…”

Characteristics of Gut Microbiota in Autoimmune Diseases of the Thyroid Gland and the Methods of Its Correction

“…The authors have suggested that it was the GM that influenced autoimmunity and may affect the development of type 1 diabetes [4]. C. aerofaciens may affect the pathogenesis of RA through various mechanisms, for example, by increasing the permeability of the intestinal wall, production of IL-17, and chemotaxis of neutrophils [6].…”