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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.
Acute kidney injury (AKI) occurs in approximately 15% of hospitalized patients and it predisposes the patients to chronic kidney disease (CKD). Interleukin-10 (IL-10) is a pleiotropic cytokine, and exogenous IL-10 replacement therapy is renoprotective effect against AKI. However, the required concentration of IL-10 seems not feasible to achieve when applied to human. Subpopulation of B cells presenting with CD1dhiCD5+ (regulatory B cells; Breg) are known to be responsible for producing and secreting IL-10. Thus, in this study, we investigated the role of Breg in AKI and whether Breg infusion and in vivo induction can prevent the AKI-to-CKD transition.
IL10+/eGFP mice were employed to trace IL-10-producing Breg in the context of AKI. Ischemia-reperfusion (IR)-AKI was induced in IL10+/eGFP mice and the number of GFP-labelled Breg were evaluated in several organs, such as kidneys and spleens. Subpopulation of B-1 cells isolated from peritoneal cavity of IL10+/eGFP mice were infused into wild-type mice with IR-AKI to examine whether exogenous regulatory B cells adhere to the injured kidneys. Third, spleen, the main source of Breg, were removed before IR-AKI to explore whether deletion of Breg exacerbates AKI in IL10+/eGFP mice. Finary, we examined whether vagus nerve stimulation(VNS) increased Breg in the spleen and kidneys, and whether it exerted a renoprotective effect.
The number of GFP+ Breg was increased in the spleens 24 hrs after onset of IR-AKI. The number of GFP+ Breg was increased in the kidneys with the upregulation of IL-10 gene expression on day7 and 14 after IR-AKI. Furthermore, when GFP+ B-1 cells were exogenously infused, we identified GFP+ cells in kidneys of wild-type mice with IR-AKI, the number of which was increased in injured kidneys and spleen. Splenectomy in the context of AKI reduced the number of GFP+ cells in kidneys of IR-AKI with the reduction in gene expression of IL-10. Renal dysfunction and tubular damage in IR-AKI were worsened by splenectomy and immune cells infiltration, such as CD68+ macrophages and CD3+ T cells, were enhanced. Furthermore, GFP+ cells increased in the kidneys and spleen at IR-AKI after VNS, and reduced renal dysfunction and tubular and interstitial damage.
We identified that IL-10-producing Breg were mainly released from the spleens in response to IR-AKI, which may be involved in repair process after IR-AKI via producing IL-10. In addition, the infusion with autologous Breg and in vivo induction of Breg by VNS might be potent to promote proper repair and prevent AKI-to-CKD.
