Probiotic supplementation improves inflammatory status in patients with rheumatoid arthritis

Abstract

Objectives: Rheumatoid arthritis (RA) is an inflammatory autoimmune disease in which the gut microbiota is altered. Probiotics are microorganisms that can normalize gut microbiota; thus, they may help to alleviate RA symptoms. The objective of the present clinical trial was to assess the effects of probiotic supplementation on disease activity and inflammatory cytokines in patients with RA. Methods: Forty-six patients with RA were assigned into two groups in this randomized, double-blind, placebo-controlled clinical trial. The patients in the probiotic group received a daily capsule that contained a minimum of 10(8) colony-forming units of Lactobacillus casei 01 for 8 wk. The placebo group took capsules filled with maltodextrin for the same time period. Questionnaires, anthropometric measurements, and fasting blood samples were collected, and the participants were assessed by a rheumatologist at baseline and at the end of the trial. Results: Disease activity score was significantly decreased by the intervention, and there was a significant difference between the two groups at the end of the study (P < 0.01). Three of the assessed serum proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, and interleukin-12) significantly decreased in the probiotic group (P < 0.05); however, serum levels of interleukin-1 beta were not significantly affected by the probiotic (P = 0.22). The serum level of regulatory cytokine (interleukin-10) was increased by the supplementation (P < 0.05). The proportion of interleukin-10 to interleukin-12 was significantly increased in the probiotic group as well. Conclusions: L casei 01 supplementation improved the disease activity and inflammatory status of patients with RA. Further studies are warranted to confirm these results, and such confirmation may lead to the introduction of probiotics as adjunctive therapy for this population. (C) 2014 Elsevier Inc. All rights reserved.