| Literature DB >> 29317279 |
Dan-Dan Liu1, Shi-Feng Chu2, Chen Chen2, Peng-Fei Yang2, Nai-Hong Chen3, Xin He4.
Abstract
In recent years, stroke-induced immunodepression syndrome (SIDS) and the resulting stroke-associated infection (SAI) have become a focus of current research efforts. Inflammatory reactions after stroke promote tissue healing and eliminate necrotic cells, whereas excessive inflammatory reactions may cause secondary damage. Stroke-induced immunodepression not only reduces inflammatory reactions and protects brain tissues but also weakens the resistance of the human body against pathogens and leads to infection. Changes in the local and systemic immune system in stroke patients may play an important role in prognosis. Infection is a leading cause of death in patients following stroke, and an evaluation of the prognosis of stroke patients is associated closely with the presence of infectious complications. Among these complications, pneumonia is the most common type of infection observed after acute stroke, which exhibits the greatest effect on the recovery of neurological function. SIDS is closely related to stroke-associated pneumonia (SAP), and the use of immunodepression as an entry point may provide an efficacious treatment target and drug development strategy. An improved understanding of the pathophysiological mechanisms leading to SAP is essential to develop new treatment strategies for improving the outcomes of stroke patients.Entities:
Keywords: Cytokines; Stroke-associated infection; Stroke-associated pneumonia; Stroke-induced immunodepression syndrome
Mesh:
Year: 2018 PMID: 29317279 DOI: 10.1016/j.neuint.2018.01.002
Source DB: PubMed Journal: Neurochem Int ISSN: 0197-0186 Impact factor: 3.921