A recent study led by Professor Arthur Liesz from the Institute for Stroke and Dementia Research (ISD) at LMU University Hospital has revealed significant findings on the long-term health impacts of strokes on systemic immunity, particularly how they affect other organs like the heart.
While the immediate brain damage from a stroke is well-documented, the research delves into the less explored territory of how brain injuries influence systemic immunity. Published in the journal Cell, this study marks a pivotal step in understanding the broader health implications of strokes.
The researchers hypothesized that the common occurrence of comorbidities following a stroke might share an immunological root.
Their findings confirmed this hypothesis, pinpointing the source of bodily dysfunctions in the altered immunological memory of bone marrow’s blood-forming cells. This discovery suggests that the immune response post-stroke triggers broader systemic changes, leading to complications in various organs.
Through single-cell sequencing, the team identified lasting proinflammatory changes in the transcriptome of specific immune cells, such as monocytes and macrophages, across multiple organs.
These changes, driven by different gene transcription post-stroke, disrupt the proteome balance and lead to epigenetic modifications. Notably, these modifications are most pronounced in the heart, causing scarring and impairing its pumping function.
A critical finding of the study is the identification of the protein IL-1b as the primary agent causing these harmful epigenetic changes affecting immunological memory after a stroke. This protein plays a significant role in the altered immune responses that lead to further health issues, particularly cardiac dysfunctions, following a stroke.
The study also highlights promising therapeutic avenues. In a mouse model, the researchers showed that blocking IL-1b and preventing the migration of proinflammatory cells to the heart can effectively prevent post-stroke cardiac problems.
These insights pave the way for developing treatments aimed at mitigating secondary cardiac conditions post-stroke, emphasizing the potential of targeting IL-1b-mediated pathways.
The authors believe that these epigenetic mechanisms could provide a new framework for understanding and treating various comorbidities that arise due to immune system reprogramming in the brain-heart axis.
