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
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