Abstract:
BACKGROUND:Interleukin-33 (IL-33) is increasingly being recognized as a key immunomodulatory cytokine in many neurological diseases. METHODS:In the present study, wild-type (WT) and IL-33-/- mice received intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS) to induce neuroinflammation. Intravital microscopy was employed to examine leukocyte-endothelial interactions in the brain vasculature. The degree of neutrophil infiltration was determined by myeloperoxidase (MPO) staining. Real-time PCR and western blotting were used to detect endothelial activation. Enzyme-linked immunosorbent assay and quantitative PCR were conducted to detect pro-inflammatory cytokine levels in the brain. RESULTS:In IL-33-/- mice, neutrophil infiltration in the brain cortex and leukocyte-endothelial cell interactions in the cerebral microvessels were significantly decreased as compared to WT mice after LPS injection. In addition, IL-33-/- mice showed reduced activation of microglia and cerebral endothelial cells. In vitro results indicated that IL-33 directly activated cerebral endothelial cells and promoted pro-inflammatory cytokine production in LPS-stimulated microglia. CONCLUSIONS:Our study indicated that IL-33/ST2 signaling plays an important role in the activation of microglia and cerebral endothelial cells and, therefore, is essential in leukocyte recruitment in brain inflammation. The role of IL-33/ST2 in LPS induced neuroinflammation.
journal_name
J Neuroinflammationjournal_title
Journal of neuroinflammationauthors
Cao K,Liao X,Lu J,Yao S,Wu F,Zhu X,Shi D,Wen S,Liu L,Zhou Hdoi
10.1186/s12974-018-1169-6subject
Has Abstractpub_date
2018-05-04 00:00:00pages
136issue
1issn
1742-2094pii
10.1186/s12974-018-1169-6journal_volume
15pub_type
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