Host Genetics May Affect Intestinal Microbiota Composition in Reactive Arthritis

In reactive arthritis (ReA), a form of postinfectious spondyloarthritis (SpA), host genetics, particularly in the human leukocyte antigen (HLA)-A24, may be associated with observed differences in gut microbiota composition vs controls, according to a study published in Arthritis & Rheumatology.

A total of 32 patients with ReA and 32 controls were enrolled prospectively from July through October 2014 in Guatemala City, Guatemala, an area with a high prevalence of ReA. All of the patients with ReA – but none of the controls – had peripheral arthritis (P <.0001), with an average tender joint count of 5. 

Study participants, age 18 to 55, all reported gastrointestinal (GI) and/or genitourinary (GU) infection in the 3 to 6 months preceding study enrollment. Diarrhea and dysuria were reported by study participants with GI and GU infections, respectively, in addition to occasional hematuria. 

Clinical variables and HLA status were assessed, and 16S ribosomal RNA (16S rRNA) gene sequencing of gut microbiota performed in all study participants.

No differences were reported in patients with ReA or controls with respect to intestinal bacterial richness or diversity. However, participants with ReA had a greater abundance of Erwinia and Pseudomonas and an increased prevalence of enteropathogens typically associated with ReA.

Ultrasound-identified Achilles enthesitis was observed with a greater prevalence in patients with ReA compared with controls (43.8% vs 6.3%, respectively; P =.0005), and these patients also presented with enriched Campylobacter. 

In addition, a higher rate of uveitis was found in patients with ReA vs controls (62.5% vs 6.3%, respectively; P <.0001), and participants with uveitis had enriched Erwinia and Dialister. Host genetics, in particular HLA-A24, were associated with differences in intestinal microbiota, regardless of disease status.

The investigators concluded that “Understanding of these gut microbiota host-genetic relationships may further clarify the pathogenesis of post-infectious spondyloarthropathies.” Several gut bacterial strains were found to be differentially expressed in samples from patients with ReA compared with controls in this study. 

Whether gut microbiota are the cause or a consequence of SpA-related inflammation warrants further clarification.

Reference

Manasson J, Shen N, Garcia Ferrer HR, et al. Gut microbiota perturbations in reactive arthritis and post-infectious spondyloarthritis [published October 26, 2017]. Arthritis Rheumatol. doi:10.1002/art.40359