Faculty Bibliography

Changes in lung microbiota associated with smoking might contribute to the development of acute respiratory distress syndrome in subjects with blunt trauma.

OBJECTIVE: Reactive arthritis (ReA) is an inflammatory disorder occurring several weeks after gastrointestinal or genitourinary infections. HLA-B27 positivity is considered a risk factor, though not necessarily predictive of disease incidence. Among non-genetic factors, the intestinal microbiome may play a role in disease susceptibility. The objective of this study was to characterize the gut microbiota and host gene interactions in ReA and post-infectious spondyloarthritis. METHODS: Adult peripheral spondyloarthritis and control subjects with preceding infections that did not develop arthritis were prospectively recruited from a highly prevalent geographic region. Clinical variables, HLA status, and 16S rRNA gene sequencing of intestinal microbiota were analyzed. RESULTS: ReA subjects showed no significant differences from controls in gut bacterial richness or diversity. However, there was a significantly higher abundance of Erwinia and Pseudomonas, and increased prevalence of typical enteropathogens associated with ReA. Subjects with ultrasound evidence of enthesitis were enriched in Campylobacter, while subjects with uveitis and radiographic sacroiliitis were respectively enriched in Erwinia and unclassified Ruminococcaceae, and both enriched in Dialister. Host genetics, particularly HLA-A24, were associated with differences in gut microbiota diversity irrespective of disease status. We determined several co-occurring taxa that were also predictive of HLA-A24 status. CONCLUSION: This is the first culture-independent study characterizing the gut microbial community of post-infectious arthritis. Although bacterial factors correlated with disease presence and clinical features of ReA, host genetics also appeared to be a major independent driver of intestinal community composition. Understanding of these gut microbiota host-genetic relationships may further clarify the pathogenesis of post-infectious spondyloarthropathies.