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Neurological Outcomes Linked to Innate Immune Features After Cardiac Arrest

In the journal Med, a team from Brigham and Women's Hospital, Harvard Medical School, St. Jude Children's Research Hospital, and other centers turn to single-cell transcriptomics to better understand neurological injury after cardiac arrest. Based on past studies suggesting neurological injury in cardiac arrest patients involves systemic inflammation, the researchers used flow cytometry and single-cell RNA sequencing to track immune-related transcriptomic patterns in nearly 96,200 peripheral blood mononuclear cells from blood samples collected as early as six hours after cardiac arrest in 11 cardiac arrest patients and three healthy control individuals. Together, the results suggest that individuals with better or worse neurological outcomes a month after cardiac arrest had distinct monocyte and natural killer cell features influencing cytokine and immune checkpoint activity, even in samples collected soon after the event. "Cardiac arrest triggers an early negative feedback loop in which pro- and anti-inflammatory cytokines induce immune checkpoints that limit inflammation," the authors suggest. "These findings support investigation of therapeutic approaches that augment protective immune mechanisms very early after cardiac arrest."

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