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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.
The MRL/lpr mouse is a representative autoimmune-prone model characterized by spontaneous inflammation and immune cell infiltration. While Toll-like receptor 4 (TLR4) activation is known to trigger strong innate immune responses, its contribution to renal parenchymal inflammation in this model remains unclear.
To examine the effect of TLR4 stimulation, a low dose of lipopolysaccharide (LPS) was intraperitoneally administered to MRL/lpr mice. Renal histology was evaluated 24 hours post-injection. Immunostaining for CD44, a marker of activated parietal epithelial cells (PECs) that is rapidly induced in crescentic glomerulonephritis, and F4/80, a macrophage marker specific to mice, was performed. In situ hybridization (ISH) for F4/80 mRNA was also conducted. Furthermore, bulk RNA sequencing was performed to profile transcriptional changes, and key upstream regulators were identified using the VIPER algorithm referencing the Dorothea regulon database, complemented by GSVA and ULM analyses.
LPS-challenged MRL/lpr mice showed marked cellular infiltration and glomerular injury compared to PBS controls. CD44 immunostaining revealed activation of PECs and Bowman’s capsule involvement only in the LPS group, consistent with an RPGN-like inflammatory pattern. F4/80 staining and ISH signals were also markedly increased in the LPS-treated kidneys, highlighting macrophage infiltration into both the interstitium and glomerular regions. Transcriptomic profiling identified multiple inflammation- and injury-related genes, including Lcn2 (NGAL), upregulated in LPS-treated kidneys. Although no novel marker genes were detected, gene regulatory network analysis consistently pinpointed Spi1 (PU.1) as the top-ranked master regulator activated by LPS stimulation across VIPER, GSVA, and ULM methods.
These findings suggest that LPS-induced TLR4 activation in autoimmune-prone MRL/lpr mice provokes PEC-associated and macrophage-mediated inflammation resembling RPGN. The consistent activation of Spi1 across computational analyses indicates its central role in orchestrating the inflammatory transcriptional program. This model thus provides a translationally relevant platform to investigate Spi1-driven inflammatory pathways and their therapeutic modulation in human glomerular diseases.
