Bacteremia persistently alters T-lymphocyte phenotypes in the murine heart 9332

Abstract Description T-lymphocytes play critical roles in cardiovascular pathologies, but whether their populations in cardiovascular tissue remain persistently altered following a severe bacterial bloodstream infection is unclear. Such alterations could influence future cardiovascular disorders. This study examined whether prior bacteremia, induced by the cecal ligation and puncture (CLP) model, leads to long-term changes in cardiac T-lymphocytes. Cardiac leukocytes were flow-sorted from mouse hearts six weeks post-bacteremia and analyzed via single-cell RNA sequencing (scRNA-seq) to assess transcriptional and compositional changes. Extensive analysis revealed significant transcriptional remodeling in T cells from CLP-treated hearts compared to controls. Several pro-inflammatory and stress-related genes, including Junb, Bcl3, Nfkbia, Socs3, Icam1, Fkbp5, and Gadd45g, were upregulated in T cells from CLP hearts. Gene ontology enrichment analysis identified pathways associated with the antimicrobial humoral immune response, neutrophil chemotaxis, granulocyte chemotaxis, neutrophil migration, and response to lipopolysaccharide, suggesting a persistent inflammatory signature in cardiac T cells. These findings indicate that bacteremia induces lasting transcriptional and compositional changes in cardiac T cells that persist beyond the resolution of infection. Further studies are needed to understand the mechanisms behind these changes and their potential impact on cardiovascular disease. Funding Sources Supported by Deutsche Forschungsgesellschaft Topic Categories Cytokines and Chemokines and Their Receptors (CCR)