HMGB1 and brain ischemia: This suggests that accumulated extracellular HMGB1 may not only mediate acute damaging processes in the brain but also aggravate inflammation in the brain and increase vulnerability to post-stroke infection (PSI) Recently, a study reported that HMGB1 can exacerbate inflammatory damage to the BBB during the process of brain ischemia–reperfusion, which may be the cause of the release of HMGB1 from the brain to the CSF and circulation (Li M. et al., 2018).