Mechanistic insights to infection after stroke for better targeted therapeutics

Bacterial lung infection is a leading cause of death in patients with stroke. Use of antibiotics as both a therapy and prevention have failed, emphasising the requirement for new therapeutics to combat this fatal complication that plagues patients with stroke. This thesis explores changes to the immune system that leaves the body prone to developing infection following a stroke. These findings show that the degree of immune suppression is dictated by the severity of stroke and increases the risk of developing infection. With this knowledge, this thesis demonstrates that specifically activating certain immune cells can effectively combat post-stroke infection.