Abstract
ObjectiveAlterations in the microbiota composition of the gastro-intestinal tract are suspected to be involved in the etiopathogenesis of two closely related systemic inflammatory autoimmune diseases: primary Sjögren's syndrome (pSS) and systemic lupus erythematosus (SLE). Our objective was to assess whether alterations in gut and oral microbiota compositions are specific for pSS and SLE. Methods16S ribosomal RNA gene sequencing was performed on fecal samples from 39 pSS patients, 30 SLE patients and 965 individuals from the general population, as well as on buccal swab and oral washing samples from the same pSS and SLE patients. Alpha-diversity, beta-diversity and relative abundance of individual bacteria were used as outcome measures. Multivariate analyses were performed to test associations between individual bacteria and disease phenotype, taking age, sex, body-mass index, proton-pump inhibitor use and sequencing-depth into account as possible confounding factors. ResultsFecal microbiota composition from pSS and SLE patients differed significantly from population controls, but not between pSS and SLE. pSS and SLE patients were characterized by lower bacterial richness, lower Firmicutes/Bacteroidetes ratio and higher relative abundance of Bacteroides species in fecal samples compared with population controls. Oral microbiota composition differed significantly between pSS patients and SLE patients, which could partially be explained by oral dryness in pSS patients. ConclusionspSS and SLE patients share similar alterations in gut microbiota composition, distinguishing patients from individuals in the general population, while oral microbiota composition shows disease-specific differences between pSS and SLE patients.
Highlights
Primary Sjögren's syndrome and systemic lupus erythematosus (SLE) are systemic inflammatory autoimmune diseases that share epidemiological, clinical, pathogenic and etiological features [1,2]
39 fecal samples from primary Sjögren's syndrome (pSS) patients, 30 fecal samples from SLE patients and 965 fecal samples from population controls were used in the analyses
The vast majority of clinical characteristics was similar between pSS patients with and without a history of salivary gland mucosa associated lymphoid tissue (MALT) tumor (Supplementary Table 1)
Summary
Primary Sjögren's syndrome (pSS) and systemic lupus erythematosus (SLE) are systemic inflammatory autoimmune diseases that share epidemiological, clinical, pathogenic and etiological features [1,2]. The world-wide prevalence rates for pSS and SLE are 0.01–0.09% and 0.02–0.24%, respectively, with a female:male ratio of 10:1 for both diseases [3,4,5,6]. Overlap of clinical symptoms is frequently observed in pSS and SLE patients [7,9,10]. PSS and SLE patients share genetic risk loci which predisposes individuals to these diseases. Genetic risk loci for both pSS and SLE include STAT4 and IRF5 (involved in innate immunity), IL12A and BLK (involved in adaptive immunity) and HLA class II region [11,12,13,14]. The majority of SLE genetic risk factors are involved in innate immune signaling (e.g. TLR7 and TLR9) and lymphocyte signaling (e.g. IL-10, CD80) [15]
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