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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 is an inflammation-driven syndrome that arises across diverse clinical settings. Despite high mortality, poor outcomes, and accelerated progression to chronic or end-stage kidney disease, mechanism-anchored, disease-specific therapies are yet to be established. In 2000, Tracey et al. first defined the cholinergic anti-inflammatory pathway (CAP), in which vagus nerve stimulation (VNS) suppresses systemic cytokine release in a sepsis (endotoxemia) model. Subsequent studies demonstrated that CAP attenuates inflammation across multiple organs, including the kidney. In this circuit, vagal efferents and the splenic nerve affect splenocytes. The spleen contributes significantly to this response, supported by findings showing that splenectomy abolished VNS-mediated anti-inflammatory and renoprotective effects and that adoptive splenocyte transfer from VNS-treated mice conferred kidney protection in VNS-naïve mice. However, the mechanism by which the splenocytes influence a distant organ such as the kidney remains unclear. This study aimed to label splenocytes in vivo and trace them after VNS to probe this unresolved mechanism.
We established an in vivo splenocyte-tracing approach in KikGR mice, in which violet illumination irreversibly photoconverts KikGreen to KikRed. Illumination parameters (wavelength, power, exposure time, working distance, and spot size) were optimized, and the final protocol employed a USHIO SP-11 (preset 275-W UV lamp) with a 365-nm band-pass filter at 100% lamp power, 20 min per side (ventral and dorsal) at a 22-mm working distance, while cooling with running water. These parameters were chosen to maximize photoconversion while preserving viability, as assessed by flow cytometry (7-AAD and Annexin V). Mice were subsequently subjected to VNS or sham treatment, photoconverted (KikRed⁺) cells were quantified by flow cytometry, and immune cell subsets were profiled in the spleen, peripheral blood, and kidney.
Using the above parameters, the efficiency of in vivo splenic photoconversion exceeded 80%, surpassing previously reported systems (~40% at most). Cell viability was unaffected; 7-AAD and Annexin V did not show any increase in dead or apoptotic cells compared with non-illuminated controls. In preliminary experiments, more CD45⁺KikRed⁺ cells (immune cells located in the spleen during illumination) were found in the kidneys of VNS-treated mice than in sham-treated mice. Ongoing work is defining which CD45⁺ subsets traffic to the kidney after VNS.
We established a high-efficiency (>80%) in vivo splenocyte-tracing platform that outperforms previously reported systems. Preliminary experiments suggest that VNS may influence renal splenocyte infiltration. This system enables exploration of the missing link between the spleen and the kidney in renoprotection mediated by VNS.
