The Intestinal Microbiome in Spondyloarthritis

Tejpal Gill; Mark Asquith; James T. Rosenbaum; Robert A. Colbert


Curr Opin Rheumatol. 2015;27(4):319-325. 

In This Article

Abstract and Introduction


Purpose of review Microbial dysbiosis in the gut is emerging as a common component in various inflammatory disorders including spondyloarthritis (SpA). The depth of this influence has begun to be realized with next-generation sequencing of the gut microbiome providing unbiased assessment of previously uncharted bacterial populations.

Recent findings Decreased numbers of Firmicutes, a major phyla of gut commensals, especially the species Faecalibacterium prausnitzii and Clostridium leptum have been found in various inflammatory disorders including SpA and inflammatory bowel disease (IBD), and could be an important link between SpA and gut inflammation. Multiple studies in ankylosing spondylitis, psoriatic arthritis, juvenile SpA, and animal models of SpA are revealing common bacterial associations among these diseases as well as IBD.

Summary We are beginning to appreciate the complex relationship between the gut microbiome and host immune regulation and dysregulation in health and disease. Potentially important differences have been revealed in SpA, but cause and effect relationships remain far from established. Many critical questions remain to be answered before we can apply new knowledge to improve therapeutics in SpA.


Spondyloarthritis (SpA) is a family of immune-mediated inflammatory disorders that includes ankylosing spondylitis (AS), psoriatic arthritis (PsA), juvenile spondyloarthritis (JSpA), and acute anterior uveitis. Undifferentiated SpA is now classified as axial or predominantly peripheral. There is considerable clinical overlap between SpA and inflammatory bowel disease (IBD), with IBD and AS exhibiting shared genetic predisposition and pathogenic mechanisms. IBD has been long associated with alterations in the gut microbiome, which may be primary or secondary factors in disease pathogenesis.[1]

Rats overexpressing HLA-B27 spontaneously develop an inflammatory disease exhibiting arthritis and colitis, thus, mimicking human SpA.[2] In common with the vast majority of IBD animal models, disease development in this model is microbiota dependent.[3] Rosenbaum and Davey[4] proposed that HLA-B27 alters the intestinal microbiome, which might be the basis for disease predisposition associated with this allele. This concept is supported by theories of a disrupted gut environment in spondyloarthropathy, with altered intestinal permeability perhaps leading to a dysregulated immune response and/or altered dendritic-cell function. This may then drive microbial dysbiosis and/or microbiota-mediated intestinal inflammation leading to epithelial permeability. Here, we review recent developments from studies of the gut microbiome in patients with AS, JSpA, and PsA as well as insights obtained from the animal models of SpA.