IL-33 Expression in the Cerebral Cortex Following Experimental Subarachnoid Hemorrhage in Rats

Abstract

Subarachnoid hemorrhage (SAH) is a pervasive and devastating condition in which inflammatory and apoptotic pathways contribute to poor outcome. Interleukin-33 (IL-33) plays a crucial role in the inflammatory and apoptotic pathways through binding of the transmembrane ST2 receptor. This study investigated the expression and cellular localization of IL-33 in the cerebral cortex after SAH in order to clarify the role of IL-33 after SAH. Sprague-Dawley rats were randomly divided into sham and SAH groups and evaluated 2, 6, and 12 h and 1, 2, 3, and 5 days after the surgery, with SAH animals subjected to prechiasmatic cistern SAH. IL-33 expression was measured by western blot analysis, real-time PCR, immunohistochemistry, and immunofluorescence. The mRNA levels of tumor necrosis factor (TNF)-α and IL-1β were also assessed. The expression of IL-33, IL-1β, and TNF-α was markedly elevated in the SAH as compared to the sham group; IL-33 was mainly localized in neurons and astrocytes and not microglia after SAH. Moreover, a significant positive association was observed between IL-33 and IL-1β expression. These findings indicate that IL-33 might play an important role in the inflammatory response following SAH.

IL-33/ST2L Signaling Provides Neuroprotection Through Inhibiting Autophagy, Endoplasmic Reticulum Stress, and Apoptosis in a Mouse Model of Traumatic Brain Injury

“…Numerous literatures identified that IL-33 is dominantly produced by endothelial cells and astrocytes but not by microglia or neurons in vitro cellar culture (Manetti et al, 2010 ; Yasuoka et al, 2011 ). Other reports revealed that IL-33 was mainly localized in astrocytes, microglia and neurons after brain injury in vivo (Huang et al, 2015 ; Gao et al, 2017 ). We speculate the reason for the discrepancy may be caused by the different experiment settings, environments between in vitro and in vivo , or because of tissue repair process after acute brain injury.…”

IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure

“…Numerous literatures identified that IL-33 is produced by endothelial cells and astrocytes but not by microglia or neurons (Manetti et al, 2010 ; Yasuoka et al, 2011 ), and its receptors are mainly expressed in microglia and astrocytes in vitro cellar culture (Yasuoka et al, 2011 ). Other reports revealed that IL-33 was mainly localized in astrocytes, microglia and neurons after brain injury in vivo (Huang et al, 2015 ; Gao et al, 2017 ). Consistent with the latter, our current results showed that IL-33 almost exclusively located in the nucleus of astrocytes, and in the cytoplasm of microglia and neurons.…”

Role of Damage Associated Molecular Pattern Molecules (DAMPs) in Aneurysmal Subarachnoid Hemorrhage (aSAH)

“…However, IL-33 has been assigned to play an inflammatory role in CNS reflecting its pleiotropic nature [ 110 , 112 ]. Huang, et al [ 113 ] have observed an increased expression of IL-33 mRNA and protein in the cerebral cortex of the rats after experimental SAH. Intriguingly, IL-33 expression colocalized with neuronal and astrocytic markers and mRNA expression of IL-33 correlated with that of IL-1β after SAH [ 113 ].…”

“…Huang, et al [ 113 ] have observed an increased expression of IL-33 mRNA and protein in the cerebral cortex of the rats after experimental SAH. Intriguingly, IL-33 expression colocalized with neuronal and astrocytic markers and mRNA expression of IL-33 correlated with that of IL-1β after SAH [ 113 ]. So, IL-1α and IL-33 represent important DAMPs implicated in neuroinflammation after experimental SAH and therefore, needs further investigations.…”