Abstract

The incidence of stroke has risen over the past decade and will continue to be one of the leading causes of death and disability worldwide. While a large portion of immediate death following stroke is due to cerebral infarction and neurological complications, the most common medical complication in stroke patients is infection. In fact, infections, such as pneumonia and urinary tract infections, greatly worsen the clinical outcome of stroke patients. Recent evidence suggests that the disrupted interplay between the central nervous system and immune system contributes to the development of infection after stroke. The suppression of systemic immunity by the nervous system is thought to protect the brain from further inflammatory insult, yet this comes at the cost of increased susceptibility to infection after stroke. To improve patient outcome, there have been attempts to lessen the stroke-associated bacterial burden through the prophylactic use of broad-spectrum antibiotics. However, preventative antibiotic treatments have been unsuccessful, and therefore have been discouraged. Additionally, with the ever-rising obstacle of antibiotic-resistance, future therapeutic options to reverse immune impairment after stroke by augmentation of host immunity may be a viable alternative option. However, cautionary steps are required to ensure that collateral ischemic damage caused by cerebral inflammation remains minimal.

Highlights

  • IntroductionStroke is a devastating cerebrovascular event that occurs upon interruption of blood flow to areas of the brain, due to blockage (ischemic stroke) or bursting/bleeding (hemorrhagic stroke) of a cerebral blood vessel

  • Stroke is a devastating cerebrovascular event that occurs upon interruption of blood flow to areas of the brain, due to blockage or bursting/bleeding of a cerebral blood vessel

  • The impact that stroke has on the immune system is complex and, as discussed, innervation of the sympathetic nervous system and HPA axis can result in an immune shift towards a T-helper 2 (TH2) response after stroke to leave the host susceptible to infections

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Summary

Introduction

Stroke is a devastating cerebrovascular event that occurs upon interruption of blood flow to areas of the brain, due to blockage (ischemic stroke) or bursting/bleeding (hemorrhagic stroke) of a cerebral blood vessel. This resulting brain damage contributes to long-lasting disabilities and multiple functional impairments. This review will attempt to describe the changes in local and systemic immunity after stroke, outline mechanisms of stroke-induced immune suppression and infection, and highlight potential therapeutic targets to reduce post-stroke complications and improve patient health

Local Immune Responses and Impairment after Stroke
Infections after Stroke
Stroke-Induced Immune Suppression
Antibiotics
Immune Modulation
Findings
Conclusions
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