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• W2896463983 abstract "<b><i>Objective:</i></b> Knowledge regarding interactions of AFB₁ with the human nervous system and how a naturally occurring level of AFB₁ could potentially induce neuroimmune dysregulation is very limited. To assess the cellular effects of AFB₁ on the human brain, we used the human microglia cell line CHME5 as a model to pinpoint its potential in vivo translation<i>.</i> <b><i>Methods:</i></b> We used the CHME5 cell line culture system, multiplex qPCR, (chemi)bioluminescence, Luminex ELISA, and flow cytometry assays to evaluate the toxic effects of a naturally occurring level of AFB₁ on human microglia. <b><i>Results:</i></b> A low concentration of AFB₁ upregulates the mRNA expression of many proinflammatory molecules, such as TLRs, MyD88, NFκB, and CxCr4, induces intracellular ATP depletion, and increases caspase-3/7 activity at different time points following exposure to the toxin. Furthermore, AFB₁-exposed microglia secreted significantly higher levels of IFN-γ and GM-CSF after treatment. We also observed a slight increase in the percentage of apoptotic microglia (annexin V⁺/PI⁻) at 48 h posttreatment. <b><i>Conclusion:</i></b> Our work confirmed that the environmentally relevant level of AFB₁ could cause an inflammatory reaction in human microglial cells that is potentially harmful or toxic to the homeostasis of the human central nervous system and might increase susceptibility to neurodegenerative diseases." @default.
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• W2896463983 date "2018-01-01" @default.
• W2896463983 modified "2023-10-16" @default.
• W2896463983 title "Human Microglial Cells Undergo Proapoptotic Induction and Inflammatory Activation upon in vitro Exposure to a Naturally Occurring Level of Aflatoxin B₁" @default.
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• W2896463983 doi "https://doi.org/10.1159/000493528" @default.
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