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Review
. 2015 Jul;27(4):319-25.
doi: 10.1097/BOR.0000000000000187.

The intestinal microbiome in spondyloarthritis

Affiliations
Review

The intestinal microbiome in spondyloarthritis

Tejpal Gill et al. Curr Opin Rheumatol. 2015 Jul.

Abstract

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.

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Conflict of interest statement

Conflicts of interest

The authors declare no conflicts of interest relevant to this work.

Figures

Figure 1
Figure 1
Host genetics, environmental triggers or inflammation may all trigger changes to the intestinal microbiota (dysbiosis). Importantly, changes to the intestinal microbiota itself may cause or contribute to inflammation. Host genetics may either create niches that promote dysbiosis, or directly alter immune responses to the ‘normal’ microbiota. These altered immune responses may manifest in hyper-active innate and adaptive immune responses that promote inflammation. Due to intimate epithelial-microbiota interactions, dysbiosis may also disrupt barrier function and intestinal homeostasis leading to inflammation, a process itself that may impair barrier integrity. Environmental triggers of dysbiosis are incompletely understood, but include diet and antibiotic use.

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References

    1. Strober W. Impact of the gut microbiome on mucosal inflammation. Trends Immunol. 2013;34:423–430. - PMC - PubMed
    1. Taurog JD, Maika SD, Satumtira N, Dorris ML, McLean IL, Yanagisawa H, Sayad A, Stagg AJ, Fox GM, Le O’Brien A, et al. Inflammatory disease in HLA-B27 transgenic rats. Immunol Rev. 1999;169:209–223. - PubMed
    1. Taurog JD, Richardson JA, Croft JT, Simmons WA, Zhou M, Fernandez-Sueiro JL, Balish E, Hammer RE. The germfree state prevents development of gut and joint inflammatory disease in HLA-B27 transgenic rats. J Exp Med. 1994;180:2359–2364. - PMC - PubMed
    1. Rosenbaum JT, Davey MP. Time for a gut check: evidence for the hypothesis that HLA-B27 predisposes to ankylosing spondylitis by altering the microbiome. Arthritis Rheum. 2011;63:3195–3198. - PMC - PubMed
    1. Backhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Host-bacterial mutualism in the human intestine. Science. 2005;307:1915–1920. - PubMed

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