<br/>Neuroinflammation is a physiological condition caused by an immune response within the central nervous system (CNS). Neuroinflammatory stress can initiate neurodegenerative mechanisms. Microglial cells are a specialized population of macrophages that reside within the CNS and coordinate specific immunological responses.<br/>Factors contributing to neuroinflammation and its influence on neurotransmission has been the topic of much research and discussion in recent years. The interaction between pesticides and neurological impact has been widely searched to address how the pesticide itself can induce affect neurotransmission or apoptosis but this research does not include the inflammatory mechanisms that microglia provide which may modulate cytotoxicity. Certain pesticides have a substantial body of evidence indicating the inflammatory response within the CNS, such as rotenone and paraquat. However, other accessible pesticides such as glyphosate have less definitive evidence on their ability to induce a neuroinflammatory response.<br/>In this study, we assessed the influence of neuroinflammatory expression on degeneration after exposure to pesticides at environmental concentrations for rotenone, paraquat and glyphosate. We utilized this data to contribute to the mechanistic understanding of glyphosate as a neurotoxin. Utilizing a co-culture model, HMC3 human microglial cells and SH-SY5Y neuroblastoma were exposed to incrementally increasing concentrations of paraquat, rotenone, and glyphosate. Endpoints assessed after exposure in the HMC3 cells were pro-inflammatory markers such as IL-1b, TNF-a and NOX2 and microglial activation (HLA-DR). In the SH-SY5Y cell model, neuronal health was assessed through viability, mitochondrial function, and cytotoxic stress. The results of this experiment indicate a elevated immunological expression in the HMC3 microglial cell from all three pesticides. The HMC3 activation, and cytokine secretion respond in a dose-dependent manner, similar to previously reported data. We also observed a decrease in viability and mitochondrial function, with a concurrent increase in cytotoxic stressors, resulting from the inflammatory response of the HMC3 cells in the co-culture. This data allows for the assessment of complex interactions between different neuronal populations in the CNS and environmental contaminants.

Implications of human microglia neuroinflammatory response due to pesticide exposure

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