Biogenic silver NPs alleviate LPS-induced neuroinflammation in a human fetal brain-derived cell line: Molecular switch to the M2 phenotype, modulation of TLR4/MyD88 and Nrf2/HO-1 signaling pathways, and molecular docking analysis

Sharma, Anshul; Sanjay,; Jaiswal, Varun; Park, Miey; Lee, Hae‐Jeung

doi:10.1016/j.bioadv.2023.213363

Cited by 5 publications

(6 citation statements)

References 85 publications

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“…20 Recent research has shown that the overexpression of HO-1 can change the function of DCs, macrophages, and regulatory T cells and induce immune regulation. 21,22 In summary, we believe that HO-1 overexpression in MSCs may play a role in synergistic immunotherapy. 23 In this study, we propose that the intravenous injection of MSCs overexpressing HO-1 inhibits inflammation and manipulates microglial polarization to improve the efficacy of MCAO therapy.…”

Section: Introductionmentioning

confidence: 85%

“… 20 Recent research has shown that the overexpression of HO‐1 can change the function of DCs, macrophages, and regulatory T cells and induce immune regulation. 21 , 22 In summary, we believe that HO‐1 overexpression in MSCs may play a role in synergistic immunotherapy. 23 …”

Section: Introductionmentioning

confidence: 85%

“…In contrast, reduced bilirubin has effective ROS‐scavenging activity against peroxides, peroxynitrites, hydroxyls, and superoxide free radicals 20 . Recent research has shown that the overexpression of HO‐1 can change the function of DCs, macrophages, and regulatory T cells and induce immune regulation 21,22 . In summary, we believe that HO‐1 overexpression in MSCs may play a role in synergistic immunotherapy 23 …”

Section: Introductionmentioning

confidence: 98%

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Human umbilical cord derived mesenchymal stem cells overexpressing HO‐1 attenuate neural injury and enhance functional recovery by inhibiting inflammation in stroke mice

Yang,

Liu,

Deng

et al. 2023

CNS Neurosci Ther

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AimsThe current evidence demonstrates that mesenchymal stem cells (MSCs) hold therapeutic potential for ischemic stroke. However, it remains unclear how changes in the secretion of MSC cytokines following the overexpression of heme oxygenase‐1 (HO‐1) impact excessive inflammatory activation in a mouse ischemic stroke model. This study investigated this aspect and provided further insights.MethodsThe middle cerebral artery occlusion (MCAO) mouse model was established, and subsequent injections of MSC, MSCHO‐1, or PBS solutions of equal volume were administered via the mice's tail vein. Histopathological analysis was conducted on Days 3 and 28 post‐MCAO to observe morphological changes in brain slices. mRNA expression levels of various factors, including IL‐1β, IL‐6, IL‐17, TNF‐α, IL‐1Ra, IL‐4, IL‐10, TGF‐β, were quantified. The effects of MSCHO‐1 treatment on neurons, microglia, and astrocytes were observed using immunofluorescence after transplantation. The polarization direction of macrophages/microglia was also detected using flow cytometry.ResultsThe results showed that the expression of anti‐inflammatory factors in the MSCHO‐1 group increased while that of pro‐inflammatory factors decreased. Small animal fluorescence studies and immunofluorescence assays showed that the homing function of MSCsHO‐1 was unaffected, leading to a substantial accumulation of MSCsHO‐1 in the cerebral ischemic region within 24 h. Neurons were less damaged, activation and proliferation of microglia were reduced, and polarization of microglia to the M2 type increased after MSCHO‐1 transplantation. Furthermore, after transplantation of MSCsHO‐1, the mortality of mice decreased, and motor function improved significantly.ConclusionThe findings indicate that MSCs overexpressing HO‐1 exhibited significant therapeutic effects against hyper‐inflammatory injury after stroke in mice, ultimately promoting recovery after ischemic stroke.

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Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 98%

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Human umbilical cord derived mesenchymal stem cells overexpressing HO‐1 attenuate neural injury and enhance functional recovery by inhibiting inflammation in stroke mice

Yang,

Liu,

Deng

et al. 2023

CNS Neurosci Ther

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“…In addition, AgNPs promoted a microglia polarization from a pro-inflammatory M1 phenotype, characterized by decreased expression of CD80, CD86, and CD68, to an anti-inflammatory M2 phenotype, characterized by increased expression of CD206 and CD163. [273] Another example of inorganic nanostructures used as M2 polarization agents is represented by gold nanostructures: dihydrolipoic acid-gold nanoclusters (DHLA-AuNCs) showed neuroprotective effects by regulating microglial polarization. [274] Results on BV2 M1-polarized microglia cells showed how DHLA-AuNCs treatment was able to significantly downregulate the mRNA expression levels of M1-like markers such as MHC-II, CD86, and iNOS, while upregulating the mRNA expression levels of M2-like markers such as Arg-1 and CD206.…”

Section: Inorganic Nanostructuresmentioning

confidence: 99%

“…In addition, AgNPs promoted a microglia polarization from a pro‐inflammatory M1 phenotype, characterized by decreased expression of CD80, CD86, and CD68, to an anti‐inflammatory M2 phenotype, characterized by increased expression of CD206 and CD163. [ 273 ]…”

Section: Nanostructures For M2 Activation Of Microglia/macrophagesmentioning

confidence: 99%

Nanomaterials as Microglia Modulators in the Treatment of Central Nervous System Disorders

Battaglini,

Marino,

Montorsi

et al. 2024

Adv Healthcare Materials

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Microglia play a pivotal role in the central nervous system (CNS) homeostasis, acting as housekeepers and defenders of the surrounding environment. These cells can elicit their functions by shifting into two main phenotypes: pro‐inflammatory classical phenotype, M1, and anti‐inflammatory alternative phenotype, M2. Despite their pivotal role in CNS homeostasis, microglia phenotypes can influence the development and progression of several CNS disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, ischemic stroke, traumatic brain injuries, and even brain cancer. It is thus clear as the possibility of modulating microglia activation has gained attention as a therapeutic tool against many CNS pathologies. Nanomaterials are an unprecedented tool for manipulating microglia responses, in particular to specifically target microglia and elicit an in situ immunomodulation activity. In this review we will focus our discussion on two main aspects: we will analyze the possibility of using nanomaterials to stimulate a pro‐inflammatory response of microglia against brain cancer and we will introduce nanostructures able to foster an anti‐inflammatory response for treating neurodegenerative disorders. The final aim is to stimulate the analysis of the development of new microglia nano‐immunomodulators, paving the way for innovative and effective therapeutic approaches for the treatment of CNS disorders.This article is protected by copyright. All rights reserved

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Molecular mechanisms of silver nanoparticle-induced neurotoxic injury and new perspectives for its neurotoxicity studies: A critical review

Yang,

Niu,

Guo

et al. 2024

Environmental Pollution

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Biogenic silver NPs alleviate LPS-induced neuroinflammation in a human fetal brain-derived cell line: Molecular switch to the M2 phenotype, modulation of TLR4/MyD88 and Nrf2/HO-1 signaling pathways, and molecular docking analysis

Cited by 5 publications

References 85 publications

Human umbilical cord derived mesenchymal stem cells overexpressing HO‐1 attenuate neural injury and enhance functional recovery by inhibiting inflammation in stroke mice

Human umbilical cord derived mesenchymal stem cells overexpressing HO‐1 attenuate neural injury and enhance functional recovery by inhibiting inflammation in stroke mice

Nanomaterials as Microglia Modulators in the Treatment of Central Nervous System Disorders

Molecular mechanisms of silver nanoparticle-induced neurotoxic injury and new perspectives for its neurotoxicity studies: A critical review

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