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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.
Gut dysbiosis has been linked to the onset and progression of obesity, a metabolic abnormality that causes immune dysregulation leading to cardio-kidney metabolic syndrome. Yet, the connection between manipulation of gut ecosystem and obesity-associated immune dysfunctions are not entirely established.
To address this, immunomodulatory potential of Bacteroides, gut bacterium associated with obesity and its complications, was tested in a mouse model of diet-induced obesity by using single-cell transcriptomic analysis of peripheral blood mononuclear cells (PBMCs). Cell type annotation, Gene set enrichment analysis, Ingenuity Pathway Analysis and Cell-cell communication analysis were applied to establish the molecular mechanism of gut–immune axis regulation.
We found that oral administration of a strain of Bacteroides selectively alleviated high-fat diet (HFD)-induced immune dysregulation, highlighted by attenuated exhaustion state in T and NK cells. Specifically, the upregulation of T cell exhaustion and IL-27 signaling pathway in Tcyt and Th cells of HFD-fed mice, respectively, was downregulated by administration of Bacteroides. For the myeloid-derived suppressor cell (MDSC), reduction of the M1 macrophage phenotype in Itgb5+ subset and induction of M2 macrophage and MDSC signatures in AngM subset were observed in HFD-fed mice. Notably, microbe intervention attenuated upregulation of genes concerning MDSC phenotypes in the AngM subset of HFD-fed mice, revealing a reversal effect on obesity-induced MDSC state. Other than a reversal effect, supplementation with Bacteroides synergistically activated B cell populations with chronic HFD. Moreover, predictions of intercellular crosstalk inferred a decline in HFD-induced communications of monocytes/macrophages with other PBMCs by Bacteroides supplementation. Microbe intervention was associated with decreased serum triglyceride levels but not with serum glucose, cholesterol or leptin concentrations.
We demonstrated that supplementation with Bacteroides reprogrammed transcriptional aberrations and immune crosstalk across circulating leukocytes in a mouse model of diet-induced obesity. These findings unveil a complete picture of obesity-associated immune dysregulation in circulating leukocytes and extend our understanding of the gut-immune axis in obesity.
