BackgroundThe assessment and characterization of the gut microbiome has become a focus of research in the area of human autoimmune diseases. Ankylosing spondylitis is an inflammatory autoimmune disease and evidence showed that ankylosing spondylitis may be a microbiome-driven disease.ResultsTo investigate the relationship between the gut microbiome and ankylosing spondylitis, a quantitative metagenomics study based on deep shotgun sequencing was performed, using gut microbial DNA from 211 Chinese individuals. A total of 23,709 genes and 12 metagenomic species were shown to be differentially abundant between ankylosing spondylitis patients and healthy controls. Patients were characterized by a form of gut microbial dysbiosis that is more prominent than previously reported cases with inflammatory bowel disease. Specifically, the ankylosing spondylitis patients demonstrated increases in the abundance of Prevotella melaninogenica, Prevotella copri, and Prevotella sp. C561 and decreases in Bacteroides spp. It is noteworthy that the Bifidobacterium genus, which is commonly used in probiotics, accumulated in the ankylosing spondylitis patients. Diagnostic algorithms were established using a subset of these gut microbial biomarkers.ConclusionsAlterations of the gut microbiome are associated with development of ankylosing spondylitis. Our data suggest biomarkers identified in this study might participate in the pathogenesis or development process of ankylosing spondylitis, providing new leads for the development of new diagnostic tools and potential treatments.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-017-1271-6) contains supplementary material, which is available to authorized users.

BackgroundSystemic lupus erythematosus (SLE) in patients from Spain is associated with intestinal dysbiosis. This study explores whether the alteration of the gut microbiome in SLE patients from China is consistent with the intestinal dysbiosis of SLE patients from Spain.ResultsThe depletion of Firmicutes and the enrichment of Bacteroidetes in SLE patients from China were consistent with the SLE patients from Spain. Furthermore, we found that nine genera of gut microbiota were SLE-related microorganisms in Chinese subjects. Genera Rhodococcus, Eggerthella, Klebsiella, Prevotella, Eubacterium, Flavonifractor and Incertae sedis were significantly enriched, while genera Dialister and Pseudobutyrivibrio were significantly depleted in SLE patients. Receiver operating characteristic analysis indicated that the nine genera have the potential to distinguish SLE patients from healthy controls.ConclusionsComparing the dysbiosis of the gut microbiome among SLE patients from China or Spain, may indicate that the gut microbiome profiles of SLE patients are more influenced by disease than ethnicity.

This study employed microbiome and metabolome analysis to explore the fecal signatures of gout patients. Fecal samples from 52 male individuals (26 healthy controls and 26 gout patients) were analyzed by 1H NMR spectroscopy and Illumina Miseq sequencing. The signatures of microbiome showed being up-regulation of opportunistic pathogens, such as Bacteroides, Porphyromonadaceae Rhodococcus, Erysipelatoclostridium and Anaerolineaceae. The signatures of metabolome were some altered metabolites which may involve uric acid excretion, purine metabolism, and inflammatory responses. Meanwhile, the correlation between discrepant metabolites and microbial taxa indicated that they could be the combined signatures of gout. This study suggests that the combined analysis of the fecal microbiome and metabolome may effectively characterize diseases.

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MicroRNAs (miRNAs) associated with Argonaute proteins (AGOs) regulate gene expression in mammals. miRNA 3’ ends are subject to frequent sequence modifications, which have been proposed to affect miRNA stability. However, the underlying mechanism is not well understood. Here, by genetic and biochemical studies as well as deep sequencing analyses, we find that AGO mutations disrupting miRNA 3’ binding are sufficient to trigger extensive miRNA 3’ modifications in HEK293T cells and in cancer patients. Comparing these modifications in TUT4, TUT7 and DIS3L2 knockout cells, we find that TUT7 is more robust than TUT4 in oligouridylating mature miRNAs, which in turn leads to their degradation by the DIS3L2 exonuclease. Our findings indicate a decay machinery removing AGO-associated miRNAs with an exposed 3’ end. A set of endogenous miRNAs including miR-7, miR-222 and miR-769 are targeted by this machinery presumably due to target-directed miRNA degradation.