Recent Advances in the Impact of Infection and Inflammation on Stroke Risk and Outcomes.

Overview

PURPOSE OF THE REVIEW: Inflammation is a key component in the pathogenesis of cerebrovascular diseases. In the past few years, the role of systemic infection and gut dysbiosis in modulating inflammation and stroke risk has been increasingly acknowledged. In this review, we synthesize contemporary literature on the effects of infection and inflammation on stroke risk and outcomes, with a focus on periodontal disease, COVID-19 infection, and gut dysbiosis. RECENT FINDINGS: Chronic and acute infections such as periodontitis and COVID-19 induce systemic inflammation that cause atherogenesis and increase cardiac injury and arrhythmias. These infections also directly injure the endothelium leading to worsened secondary inflammation after stroke. Gut dysbiosis engenders a pro-inflammatory state by modulating intestinal lymphocyte populations that can traffic directly to the brain. Additionally, post-stroke immune dysregulation creates a compounding feedback loop of further infections and gut dysbiosis that worsen outcomes. Recent advances in understanding the pathophysiology of how infection and dysbiosis affect the progression of stroke, as well as long-term recovery, have revealed tantalizing glimpses at potential therapeutic targets. We discuss the multidirectional relationship between stroke, infection, and gut dysbiosis, and identify areas for future research to further explore therapeutic opportunities.