on the Mechanism and Treatment of Poststroke Infection

Infection International Vol.5, No.3 201669ReviewProgress in Research on the Mechanism and Treatment of Post-stroke InfectionHongtao ZhangDepartment of Internal Medicine, Qingzhou Municipal Hospital, Qingzhou ChinaKeywordsstroke; infection; immune; inflammation; reviewCorrespondenceHongtao Zhang,E-mail: zhanght@: 10.1515/ii-2017-0134AbstractPost-stroke infection hinders the recovery of stroke patients and can even cause death.

The main mechanism of post-stroke infection is related with the post-stroke center, the

activation of the peripheral immune system, and the release of inflammatory factors caused

by the lesion area and pathophysiological changes in the body. Therefore, elucidating the

body’s abnormal immune inflammatory responses after stroke is crucial for the prevention,

treatment, and alleviation of post-stroke -stroke secondary injury is an important factor that affects

the prognosis of patients. Post-stroke infection is the most

common and deadly complication of stroke. In 2006, Vargas

et al.

[1] proposed the concept of stroke-associated infection

(SAI), and that pneumonia, urinary tract infections, and

sepsis are the main factors that hinder the rehabilitation of

patients and even cause death. The immune inflammatory

response induced after stroke is an independent risk factor

for the occurrence of SAI in patients. The main presentations

of SAI are the activation of dendritic cells, macrophages,

other antigen-presenting cells, and T and B lymphocytes, as

well as the imbalanced secretion of pro-inflammatory/anti-inflammatory factors. This paper provides a review of the

pathophysiological changes associated with post-stroke

infections to provide new ideas for the prevention of post-stroke infection.

after cerebral ischemia. Although this pathway is usually

inactive, after brain injury, T-lymphocyte surface cytokine

receptor intracellular region JAK are activated to catalyze

the phosphorylation of STAT with the SH2 structural

domain. Relevant cytokine genes, such as IL-6R and IL-4R, are activated to produce an immune response cascade

reaction

[3]. The activation of the JAK/STAT pathway could

lead to the activation of glial cells and T and B lymphocytes,

as well as upregulate the expression of IFN-γ, IL-6, and

other immune inflammatory factors

[4]. Current studies

remain focused on the roles of the JAK/STAT pathway in

cardiovascular diseases and tumors. The immune response

produced by the pathway after stroke still requires further

/Fasl pathway

Fas is widely expressed in the surfaces of cell membranes and

is also known as apoptotic protein-1 or CD95 molecule. Fas

belongs to the tumor necrosis factor/nerve growth factor

receptor family. The role of Fas in immune adjustment in

the lung, liver, and other organs has been widely studied.

Recent studies

[5] have found that the Fasligand (Fasl), which

extensively exists in microglia, astrocytes, lymphocytes,

natural killer cells, monocytes, and other immune cells, is

highly expressed after brain injury and produces immune

inflammatory responses. At the same time, Fas1 and Fas

combine via cross-linking to form a trimer or multimer,

Relevant Pathways of Post-stroke

InfectionJanus Protein Tyrosine Kinase/Signal Transducer and

Activator of Transcription PathwayThe Janus protein tyrosine kinase (JAK)/signal transducer

and activator of transcription (STAT) signaling pathway has

become widely studied in recent years. Recent studies have

shown that the JAK2/STAT pathway is an important signal

transduction pathway in immune inflammatory response