Neuroprotective role of the innate immune system by microglia

Glezer, Isaías; Simard, Alain R.; Rivest, Serge

doi:10.1016/j.neuroscience.2007.02.055

Cited by 320 publications

(229 citation statements)

References 101 publications

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“…However, investigators have reported that in the event of spinal cord injury and ischemic stroke, these cells act as the surveillance system to combat inflammatory cells, secrete various neurotropic factors and anti-inflammatory cytokines (e.g. TGF␤, IL-10), remove cellular debris and oxidized molecules generated from the CNS damage, enhance cell proliferation and differentiation, and eventually maintain the homeostasis of the neural environment (42)(43)(44)(45)(46)(47). The mechanisms that dictate the functional outcomes that are related to either destructive neurodegenerative phenotypes or neuroprotective tissue repair phenotypes need to be clarified, especially with regard to the role of glial cell activation.…”

Section: Discussionmentioning

confidence: 99%

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Yueh

Chen

Nguyen

et al. 2014

Journal of Biological Chemistry

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Background: Neonatal jaundice with dangerously high levels of serum bilirubin leads to neurological toxicity. Results: Toll-like receptor 2 signaling is essential for regulation of glia activation, neuroinflammation, and oxidative stress when neonatal mice experience severe hyperbilirubinemia. Conclusion: Toll-like receptor 2 signaling is linked to a protection mode against serum bilirubin-induced brain toxicity. Significance: Understanding how signaling from innate immunity contributes to bilirubin-induced pathology.

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Section: Discussionmentioning

confidence: 99%

Developmental Onset of Bilirubin-induced Neurotoxicity Involves Toll-like Receptor 2-dependent Signaling in Humanized UDP-glucuronosyltransferase1 Mice

Yueh

Chen

Nguyen

et al. 2014

Journal of Biological Chemistry

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“…Astrocytes and microglial cells are involved in the local innate immune response triggered by various stressors (33,22). Certain functions of astrocytes and microglia are ambiguous (34). When activated, microglial cells rapidly migrate to the sites of brain damage and clear debris to maintain the integrity of the central nervous system (35,36).…”

Section: Discussionmentioning

confidence: 99%

Protective role of isoflurane pretreatment in rats with focal cerebral ischemia and the underlying molecular mechanism

Xiao

Ren

Yang

et al. 2012

Molecular Medicine Reports

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Abstract. Inflammation and immunity are important in the pathogenesis of cerebral ischemia. Toll-like receptor 4 (TLR4) is involved in the inflammatory responses of injured brain tissues. Emerging studies have focused on the effect of isoflurane (ISO) pretreatment on cerebral ischemia, however, the association between ISO pretreatment and TLR4 during cerebral ischemia remains to be elucidated. In the present study, the protective role of ISO pretreatment in rats with focal cerebral ischemia reperfusion was investigated and the molecular mechanism was discussed. Using a middle cerebral artery occlusion (MCAO) model, triphenyltetrazolium chloride staining was utilized to measure the infarct volume and brain edema and immunofluorescence staining was used to detect the MCAO-induced TLR4 expression and localization. Western blot analyses were conducted to quantify the protein expression levels of TLR4, myeloid differentiation primary response 88 (MyD88) and nuclear factor (NF)-κB in ischemic brain tissue at different time points. The results demonstrated that, following ISO pretreatment, the neurological deficits, brain edema and cerebral infarct size caused by ischemia/reperfusion were attenuated. The astrocyte and microglial activation in the brain tissue was decreased. In addition, the expression levels of TLR4, MyD88 and NF-κB were decreased. The present study indicated that ISO pretreatment may protect the brain from ischemic damage by downregulating the expression levels of TLR4, MyD88 and NF-κB.

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“…Although these steroids can directly promote stability of the BRB, their anti-inflammatory actions surely contribute to their effectiveness. Glucocorticoids blunt the inflammatory response of cells, including microglia, by a number of mechanisms [9]. Glucocorticoid treatment greatly increases the phagocytic activity of monocytes and macrophages [72,73].…”

Section: Microglial Activation In Diabetic Retinopathymentioning

confidence: 99%

“…Because activated microglia are invariably associated with acute neural damage and with chronic neurodegeneration [6], it was surmised that these cells play a detrimental causal role in neuronal diseases [7,8]. In fact, the understanding of the role of microglia in both acute and chronic CNS diseases is evolving to consider that microglial activation often represents a beneficial adaptive response to damage that is directed toward eventual resolution of disorder [9][10][11]. The view of microglia has gone so far as to consider them as necessary contributors to neuronal homeostasis such that dysfunction of their protective and corrective abilities could be causal in neurodegeneration [10].…”

Section: Introductionmentioning

confidence: 99%