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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Exogenous antigens are implicated in the pathogenesis of IgA nephropathy (IgAN), and our recent studies demonstrated that antigenic stimulation of the upper respiratory mucosa induces the production of nephritogenic IgA antibodies. Although several previous studies have analyzed the oral microbiome of IgAN patients, specific microorganisms responsible for the disease have not yet been identified. One possible reason is that these studies relied on 16S rRNA sequencing, which is not a truly comprehensive analytical approach.
To address this limitation, we conducted one of the deepest shotgun metagenomic sequencing of the oral microbiome to identify potential microbial contributors.
Saliva samples were collected from 57 patients with IgAN, 39 with chronic tonsillitis, and 29 healthy individuals. Shotgun metagenomic sequencing was performed on extracted DNA, generating a large number of 150-base-pair short reads. Universal single-copy marker genes were used to profile bacterial species and their relative abundances. Additionally, using an informatics approach based on de novo assembly, these short reads were computationally assembled into contiguous sequences (contigs) of several kilobases in length. The assembled contigs were classified into three categories—chromosome, plasmid, and phage—based on genomic features. The diversity and abundance of the contigs were then compared among categories.
Shotgun sequencing yielded an average of 67 million paired-end short reads per sample. After removing human genomic sequences, over 30 million reads per sample remained for analysis, representing the deepest oral metagenomic dataset reported to date.
When we analyzed the relative abundances of bacterial species, several taxa were significantly increased in IgAN patients compared with chronic tonsillitis patients or healthy individuals. However, there were no bacterial species consistently enriched in IgAN patients across comparisons.
In contrast, contig-based analysis revealed that several plasmid-derived contigs were significantly increased in IgAN patients. Further host prediction analysis demonstrated that these plasmids, which were enriched in IgAN patients, originated exclusively from a single bacterial genus. Notably, the increase in these plasmids was consistent across all comparisons. (Fig.1). Furthermore, the host bacteria of these plasmids were not increased in IgAN patients, suggesting that the plasmids expanded independently of their hosts.
To validate these findings, the host bacteria of these plasmids were cultured from the saliva of IgAN patients and healthy individuals. Long-read sequencing confirmed that only the isolates from IgAN patients harbored these plasmids. It is therefore possible that transformed bacteria carrying these plasmids contribute to the production of nephritogenic IgA antibodies (Fig.2). Unlike previous studies focusing on bacterial species, our findings highlight that plasmids—mobile genetic elements within the commensal microbiome—may play a critical role in the pathogenesis of IgAN.
Deep shotgun metagenomic analysis revealed that specific bacterial plasmids were significantly increased in the oral cavity of IgAN patients.
We believe that our data facilitate the development of not only non-invasive diagnostic biomarkers but also novel therapeutic strategies targeting the plasmid-associated mechanisms.
