From Lungs to Heart: scRNA-seq Illuminates Post-Pneumonia Cardiovascular Risks

Pneumonia significantly increases the risk of cardiovascular events, yet the molecular mechanisms driving this association remain poorly understood. In this study, we investigate the interplay between pneumonia and atherosclerosis by employing single-cell RNA sequencing (scRNA-seq) following murine modeling of bacterial pneumonia alongside human patient data. ApoE-deficient mice on a high-fat diet were infected with Streptococcus pneumoniae , and immune and vascular cell responses were profiled at acute (48 hours) and recovery (35 days) timepoints post-infection. This approach allowed us to map cell-type specific transcriptional signatures, identify key pathways dysregulated during infection and convalescence, identify biomarkers and model disease progression. Preliminary results suggest that pneumonia induces persistent tissue-specific cellular stress responses and inflammatory signatures that may contribute to chronic vascular remodeling and heightened cardiovascular risk. To bridge the gap between mouse and human data, we are analyzing peripheral blood mononuclear cells (PBMCs) of patients from the LIFE-Heart cohort with a documented history of pneumonia and subsequent cardiovascular events. scRNA-seq of human PBMCs is used to uncover immunological mediators that could link respiratory infections to vascular pathology. This integrative, cross-species approach combines expertise in infectious disease, cardiovascular biology, and computational analysis to uncover molecular mechanisms by which pneumonia may trigger or aggravate cardiovascular disease. The insights gained could pave the way for the development of diagnostic biomarkers and targeted therapies for individuals at increased risk following a pulmonary infection. Publication History Article published online: 04 March 2026 © 2026. Thieme. All rights reserved. Georg Thieme Verlag KG Oswald-Hesse-Straße 50, 70469 Stuttgart, Germany