Microbiota and arthritis: correlations or cause?Bravo-Blas, Alberto; Wessel, Hannah; Milling, SimonCurrent Opinion in Rheumatology: March 2016 - Volume 28 - Issue 2 - p 161–167 doi: 10.1097/BOR.0000000000000261 IMMUNOPATHOGENESIS AND TREATMENT OF AUTOIMMUNE DISEASES: Edited by Iain McInnes Abstract Author Information Purpose of review: The microorganisms that colonise our bodies, the commensal ‘microbiota’, respond to changes in our behaviour and environment, and can also profoundly affect our health. We can now investigate these organisms with unprecedented depth and precision, revealing that they may contribute to the pathogenesis of diseases including arthritis. Here we discuss the changes occurring in the microbiota in people with arthritis, and how manipulation of the microbiota may provide an additional pathway for therapy. Recent findings: We highlight two important aspects of the recent literature. First we describe changes in the microbiota identified in people with arthritis; these correlations give insights into the microbial changes that may contribute to symptoms of arthritis. We then discuss attempts to ameliorate arthritis by manipulating the microbiota. This is a rapidly developing area of research. There are tantalising hints that interventions targeting the microbiota may become therapeutically viable for some types of inflammatory arthritis. Summary: Our commensal microbial communities respond to changes in our health, and are altered in people with arthritis. Understanding the complex relationships between the microbiota and the body may enable us to deliberately manipulate these organisms and provide additional therapeutic options for people with arthritis. Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, UK Correspondence to Simon Milling, Sir Graeme Davies Building, University of Glasgow, 120 University Place, Glasgow G12 8TA, UK. Tel: +44 141 330 6419; e-mail: email@example.com Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.