scholarly journals Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells

2011 ◽  
Vol 8 (3) ◽  
pp. 265-275 ◽  
Author(s):  
Mingyong Wang ◽  
Yue Chen ◽  
Yani Zhang ◽  
Liyun Zhang ◽  
Xiao Lu ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Secretion ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Mannan Binding Lectin ◽  
Binding Lectin

OR.44. Toll-like Receptor 4 Engagement Blocks Inflammatory Cytokine Production by B Cells from Inflammatory Disease Patients

2009 ◽  
Vol 131 ◽  
pp. S21
Author(s):  
Madhumita Jagannathan ◽  
Hyunjin Shin ◽  
Yue Zhang ◽  
Hatice Hasturk ◽  
Alpdogan Kantarci ◽  
...  
Keyword(s):  
B Cells ◽  
Inflammatory Disease ◽  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Inflammatory Cytokine Production

scholarly journals Propofol Ameliorates Ischemic Brain Injury by Blocking Toll-like Receptor 4-dependent Pathway and Suppressing Consequent Inflammatory Cytokine Production

2020 ◽  
Author(s):  
Kazuha Mitsui ◽  
Masakazu Kotoda ◽  
Sohei Hishiyama ◽  
Ayasa Takamino ◽  
Sho Morikawa ◽  
...  
Keyword(s):  
Brain Injury ◽  
Inflammatory Cytokine ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Neuroprotective Effects ◽  
Inflammatory Cytokine Production ◽  
Ischemic Brain ◽  
Dependent Pathway

Abstract BackgroundIschemic stroke is one of the leading causes of mortality and morbidity worldwide. Accumulated evidence suggests that the consequent excessive inflammation plays detrimental roles in the pathogenesis of secondary injury after cerebral infarction and exacerbates the brain tissue damage. Although regulation of the inflammation would be the potential strategy for the novel treatment option, effective methods that control the cerebral inflammation have not yet been established. Recent studies have suggested that propofol, a sedative agent widely used for management of patients with acute stroke, suppresses excessive inflammation and may have neuroprotective effects against ischemic brain injury. However, the available evidence is still limited and controversial, and the underlying mechanism remains unclear. This study aimed to investigate the neuroprotective effects of propofol against ischemic brain injury, with a specific focus on Toll-like receptor 4 (TLR4), the critical mediator of inflammation in the ischemic brain.ResultsTreatment with propofol significantly reduced infarct volume in wild-type mice (7.9 ± 1.4 vs. 12.6 ± 1.1 mm3, n = 10 each, p < 0.05). The propofol-treated mice exhibited lower levels of pro-inflammatory cytokine expressions compared with the control mice (IL-6: 0.57 ± 0.23 vs. 1.00 ± 0.39, p < 0.05, IL-1β: 0.53 ± 0.24 vs. 1.00 ± 0.36, p = 0.087, n = 15 each). The neuroprotective effect of propofol was abrogated by TLR4 gene knockout. Propofol treatment had no significant effects on hemodynamic parameters.ConclusionsPropofol attenuates brain injury by blocking the TLR4-dependent pathway and suppressing pro-inflammatory cytokine production. This insight into the mechanism underlying the neuroprotective effect of propofol against ischemic brain injury may lead to a new strategy for preventing exacerbation of cerebral infarction.

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