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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.
Septic acute kidney injury (AKI) is a major complication of sepsis, and we have shown that the toll-like receptor (TLR) 9-IL-17 pathway contributed to the development of septic AKI. CpG-oligodeoxynucleotides (ODNs) are specific ligands for TLR9 and have been reported to improve survival and reduce bacterial titers when administered before sepsis. We observed that CpG-ODN administration induced marked splenomegaly in mice, peaking around day 7. This study investigated the mechanism of CpG–ODN–mediated protection, focusing on the role of splenic responses.
Male C57BL/6J, TLR9 knockout (KO), and IL-17 KO mice received intraperitoneal CpG-ODN or vehicle 7 days before sepsis induction by cecal ligation and puncture (CLP). Kidney function was assessed by serum blood urea nitrogen (BUN) 18 h after CLP, and survival was subsequently monitored. Splenic Lineage⁻ Sca-1⁺ c-Kit⁺ (LSK) cells, representing hematopoietic stem cell-enriched populations, were quantified by flow cytometry 7 days after CpG-ODN administration. To determine the contribution of the spleen and LSK cells, mice underwent splenectomy or total body irradiation (TBI) for LSK cell depletion before CpG-ODN treatment and CLP.
CpG-ODN pretreatment induced significant splenomegaly (mean 191mg in CpG-ODN group vs. 71mg in vehicle group, P < 0.0001) and increased splenic LSK cell counts (mean 1,052,854 vs. 56,683 cells, P < 0.0001). These effects were not observed in TLR9 KO or IL-17 KO mice, confirming dependence on TLR9- and IL–17–dependent pathways. CpG-ODN pretreatment significantly improved survival after CLP and reduced BUN levels (39.6 vs. 62.7 mg/dL, P = 0.00065). In contrast, no survival benefit of CpG-ODN pretreatment was observed in TLR9 KO or IL-17 KO mice. Importantly, splenectomy or TBI for LSK cell depletion abolished the survival advantage conferred by CpG-ODN, suggesting that the mobilization of LSK cells in the spleen is essential for protection.
Pretreatment with CpG-ODN improves sepsis survival and preserves kidney function, potentially through TLR9-IL-17-dependent immune pathways and mobilization of splenic LSK cells. These findings identify a novel immunomodulatory pathway that may inform therapeutic strategies to improve sepsis outcomes.
