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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 …