Stroke-induced immunosuppression and poststroke infection

Abstract

Infections occur commonly after stroke and are strongly associated with an unfavourable functional outcome of these patients. Approaches for effective management of poststroke infection remain scarce, presenting an urgent need for preventive anti-infection strategies for patients who have suffered a stroke. Emerging evidence indicates that stroke impairs systemic immune responses and increases the susceptibility to infections, suggesting that the modification of impaired immune defence could be beneficial. In this review, we summarised previous attempts to prevent poststroke infections using prophylactic antibiotics and the current understanding of stroke-induced immunosuppression. Further elucidation of the immune mechanisms of stroke will pave the way to tailored design of new treatment to combat poststroke infection via modifying the immune system.

Keywords: infection; post-stroke immunosuppression; stroke.

Figure 1

Schematic diagram of mechanisms of stroke-induced immunosuppression with NK cells as an example. In the early stages of stroke (<24 hours), ischaemic neuron-recruited NK cells are swiftly mobilised into ischaemic areas, where they promote neuronal death (not shown in figure). Subsequently (>48 hours?), ischaemic neuron-derived signals can turn off NK cells that express neurotransmitter receptors. At the peripheral level, ischaemic brain injury influences the sympathetic, parasympathetic (vagus nerve) and/or hypothalamic-pituitary-adrenal (HPA) axis systems that suppress NK cell-mediated immunity. Differences in the spectrum of neurogenic innervations, immune cell subsets and soluble mediators in the CNS versus the periphery may differentially affect _NK cell deficiency in these two compartments. BBB, blood brain barrier; BDNF, brain-derived neurotrophic factor; CNS, central nervous system; EGF, epithelial growth factor; GABA, gamma-aminobutyric acid; NK, natural killer; UTP, uridine triphosphate.