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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.
Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide, characterized with IgA-ICs deposition to the mesangial area of the glomeruli. Although its pathophysiology remains incompletely understood, it is thought that nephritogenic properties of IgA1 are thought to be secreted by B cells originating or residing in mucosa-associated lymphoid tissues (MALT), such as Gut-ALT (GALT) and Nasopharynx-ALT (NALT). IgA production in MALT is believed to interact with the mucosal bacterial flora. Recently, “short-chain fatty acids (SCFAs)”, a metabolite of bacterial origin, have been reported to affect IgA production in MALT. Here, we used a dextran sulfate sodium (DSS)-induced chronic colitis mice model with high IgA (HIGA) to show the effects of inflammation of gut-associated lymphoid tissue on the microbiota, SCFA, mucosal IgA production, and renal glomeruli.
Fourteen-week-old female HIGA mice were divided into two groups; control and DSS administration groups. DSS was dissolved in sterilized drinking water and administered in three cycles for seven days at 14 days interval. Intestinal microorganisms were analyzed using 16s rDNA sequencing, and SCFA were measured using GC/MS. Serum and fecal IgA levels were measured using enzyme-linked immunosorbent assays (ELISA). IgA glycosylation were analyzed by lectin ELISA using Ricinus communis agglutinin I (RCAI) and Sambucus nigra agglutinin (SNA). The glomerular deposition rates of IgA and IgG in renal specimens were measured using immunofluorescence.
DSS administration changed the intestinal microbiota and decreased the intestinal propionate concentration (P = 0.0291). DSS administration increased IgA secretion into the intestinal lumen and significantly decreased its reactivity with RCAI compared to the control (P = 0.0175). The glomerular deposition rates of IgA and IgG were significantly increased in the DSS group (P = 0.0070 and P = 0.0175, respectively).
DSS-induced colonic inflammation decreased intestinal propionate and increased intestinal production of degalactosylated IgA and induced glomerular IgA-IgG deposition. Further studies are needed to clarify the relationship between these findings.
