Ischemic stroke and infection: A brief update on mechanisms and potential therapies

[Display omitted] Ischemic stroke triggers a multifaceted inflammatory response in the brain that contributes to secondary brain injury and infarct expansion. In parallel with brain inflammation, ischemic stroke also leads to post-stroke immunosuppression. Stroke-induced leukopenia then predisposes patients to opportunistic infections potentially leading to pneumonia or unrinary tract infections and a worsened stroke outcome. There is evidence that the hypothalamic–pituitaryadrenal axis plays an important role in the etiology of post-stroke immunosuppression, by which prolonged glucocorticoid signalling leads to changes in immune responses. While opportunistic microbes in hospitals have been thought to be the source of infection, recent studies have reported that gut flora may also be a cause of post-stroke infection as a consequence of compromised integrity of the gut barrier after stroke. While antimicrobial drugs would appear to be a rational form of treatment for bacterial infections in stroke patients, the rise in drug-resistant bacteria and possible adverse effects of disrupting beneficial gut flora represent major challenges with these drugs. Considering the prominent role of gut microbiota in modulating immune responses, protecting and restoring the post-stroke gut bacteriome may provide significant benefit in the context of post-stroke infection. With such broad aspects of post-stroke infection occurring together with an extensive inflammatory response in the brain, a carefully considered administration of therapies for ischemic stroke is warranted.