The regulatory role of Toll-like receptors after ischemic stroke: neurosteroids as TLR modulators with the focus on TLR2/4

Tajalli-Nezhad, Saeedeh; Karimian, Mohammad; Beyer, Cordian; Atlasi, Mohammad Ali; Tameh, Abolfazl Azami

doi:10.1007/s00018-018-2953-2

Cited by 64 publications

(75 citation statements)

References 205 publications

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“…Toll-like receptors are present on both immune cells and neural cells including microglia, astrocytes, and oligodendrocytes; they provide a link between the immune and central nervous systems. The neuroinflammatory response after cerebral ischemia activates the microglia-mediated TLR signaling, and this subsequently increases the release of inflammatory cytokines and exacerbates neural damage in the acute phase of stroke ( 106 ). The negative effect of TLR signaling in neuro-regeneration has been shown in some existing studies.…”

Section: Alterations In Brain-resident Immune Cells Can Promote Neuromentioning

confidence: 99%

Communications Between Peripheral and the Brain-Resident Immune System in Neuronal Regeneration After Stroke

et al. 2020

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Cerebral ischemia may cause irreversible neural network damage and result in functional deficits. Targeting neuronal repair after stroke potentiates the formation of new connections, which can be translated into a better functional outcome. Innate and adaptive immune responses in the brain and the periphery triggered by ischemic damage participate in regulating neural repair after a stroke. Immune cells in the blood circulation and gut lymphatic tissues that have been shaped by immune components including gut microbiota and metabolites can infiltrate the ischemic brain and, once there, influence neuronal regeneration either directly or by modulating the properties of brain-resident immune cells. Immune-related signalings and metabolites from the gut microbiota can also directly alter the phenotypes of resident immune cells to promote neuronal regeneration. In this review, we discuss several potential mechanisms through which peripheral and brain-resident immune components can cooperate to promote first the resolution of neuroinflammation and subsequently to improved neural regeneration and a better functional recovery. We propose that new insights into discovery of regulators targeting pro-regenerative process in this complex neuro-immune network may lead to novel strategies for neuronal regeneration.

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Section: Alterations In Brain-resident Immune Cells Can Promote Neuromentioning

confidence: 99%

Communications Between Peripheral and the Brain-Resident Immune System in Neuronal Regeneration After Stroke

et al. 2020

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“…Phylogenetic analysis of the TLR10 isolates were analyzed by macrogen and compared with sequences of different TLR10 available in a Gen Bank database, there is no convergence between our TLR10 isolates and that of the Gen Bank database. As seen in figure (15).…”

Section: Phylogenetic Tree Analysis For Tlr10mentioning

confidence: 87%

“…( Amer, et al,2014) As far as their studies and our findings are concerned, the expression of all tlrs should undoubtedly increase with inflammatory grades. ( Tajalli , et al,2019) their review focused on aspects of TLR signaling during acute neuropathological challenges in the brain and highlighted the potential neuroprotective capacity of estrogen, progesterone and vitamin D3 and their putative interactions with TLR signaling pathways after cerebral ischemia and TBI. In particular, TLR2 and TLR4 signaling appeared to be pivotal for controlling pathogenic immune responses following stroke.…”

Section: Discussionmentioning

confidence: 99%

Molecular Gene Expression of Toll-Like Receptors 4 & 10 in Cellular Subsets of Human Peripheral Blood among Patients with Prostatitis: Conventional, Real Time Pcr and DNA Sequencing Techniques

Alsaimary

AlDhaheri

Almusafer

2020

ijmsci

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The Aim of this study was to determine Immunogenetic expression of Toll-like receptor gene clusters related to prostatitis, to give acknowledge about Role of TLR in prostatitis immunity in men from Basrah and Maysan provinces. A case–control study included 135 confirmed prostatitis patients And 50 persons as a control group. Data about age, marital status, working, infertility, family history and personal information like (Infection, Allergy, Steroid therapy, Residency, Smoking, Alcohol Drinking, Blood group, Body max index (BMI) and the clinical finding for all patients of Prostatitis were collected , The molecular expression study include extracting DNA from blood of Prostatitis patients , Prostitis patients and Control group by using specific primers for conventional PCR and Real Time PCR , the amplification of all extracted DNA from blood samples was preform and confirm by using electrophoresis with (100volt/30min). The amplification of all extracted DNA from blood samples was preform and confirm by using electrophoresis with (100volt/30min) , the result of this estimation revealed that the amplified DNA(PCR product) was 227bp for TLR4 on agarose gel (1%) , (50voltage for 1hour ) with a presence 100% , (PCR product) was 279bp for TLR10 on agarose gel(1%) , (50volt/1hour) with a presence 80%. The results of the present study indicate that the Toll like receptor alleles associated with risk of prostatitis.

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“…Stimulation of TLR4 can further trigger a phosphorylation cascade leading to activating NF‐κB, the main transcription factor implicated in the TLR4 pathway. M1 Microglia can be activated via TLR4/NF‐κB pathway, leading to further inflammatory injury (Peng et al, ; Shi et al ; Tajalli‐Nezhad, Karimian, Beyer, Atlasi, & Azami Tameh, ). The detrimental role of TLR4/NF‐κB signaling pathway in experimental SAH has been established before (Wang ).…”

Section: Discussionmentioning

confidence: 99%

Biglycan regulates neuroinflammation by promoting M1 microglial activation in early brain injury after experimental subarachnoid hemorrhage

Xie

Peng

Pang

et al. 2019

Journal of Neurochemistry

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Neuroinflammation can be caused by various factors in early brain injury after subarachnoid hemorrhage (SAH). One of the most important features of this process is M1 microglial activation. In turn, the TLR4/NF-κB pathway plays an essential role in activating M1 phenotypic microglia. Biglycan, a small leucine-rich proteoglycan, functions as an endogenous ligand of TLR4 and TLR2 in macrophages. However, the underlying mechanisms associated with microglial activation in stroke pathogenesis are poorly understood. Here, we aimed to identify the role of biglycan in neuroinflammation following SAH. In our study, SAH was induced by endovascular perforation in young male C57BL/6J mice. Lentiviral vector was administered intracerebroventricularly to knock down Biglycan. Post-SAH assessments included neurobehavioral tests, immunofluorescence, western blot, qRT-PCR, Co-IP, flow cytometry, and ELISA. The biglycan level was markedly elevated following SAH in vivo. Of particularly note, knockdown of biglycan significantly improved neurological outcomes.TLR4 was bound with soluble biglycan in vitro. In addition, biglycan down-regulation suppressed the expression of phosphorylated-NF-κB p65 (p-NF-κB) and inducible nitric oxide synthase (iNOS), as well as the cytokine (TNF-α, IL-1β, and IL-6) production in vivo and in vitro. Moreover, we detected a decreased expression of CD16/32 and CD86, M1 markers when biglycan was inhibited in vitro. Our work suggests that biglycan can induce neuroinflammation by promoting M1 microglial activation at least in part through TLR4/NF-κB signaling pathway after experimental SAH. Targeting biglycan may be a promising strategy for the clinical management of SAH. K E Y W O R D Sbiglycan, early brain injury, microglia, neuroinflammation, subarachnoid hemorrhage, TLR4 | 369 XIE Et al.

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The regulatory role of Toll-like receptors after ischemic stroke: neurosteroids as TLR modulators with the focus on TLR2/4

Cited by 64 publications

References 205 publications

Communications Between Peripheral and the Brain-Resident Immune System in Neuronal Regeneration After Stroke

Communications Between Peripheral and the Brain-Resident Immune System in Neuronal Regeneration After Stroke

Molecular Gene Expression of Toll-Like Receptors 4 & 10 in Cellular Subsets of Human Peripheral Blood among Patients with Prostatitis: Conventional, Real Time Pcr and DNA Sequencing Techniques

Biglycan regulates neuroinflammation by promoting M1 microglial activation in early brain injury after experimental subarachnoid hemorrhage

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