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Published on: June 10, 2020
Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.
Dhruba Pathak1, Krishnan Sriram1
1Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Occupational injuries and toxicants trigger neuroinflammation and reactive gliosis, impacting brain function and leading to neurological disorders. Understanding these molecular signaling pathways is crucial for preventing and treating related diseases.
Area of Science:
- Neuroscience
- Toxicology
- Immunology
Background:
- Occupational injuries and toxicant exposures initiate neuroinflammation via distinct signaling cascades.
- Reactive gliosis, glial cell activation, plays a key role in central nervous system (CNS) injury progression.
- Limited understanding exists regarding the molecular mechanisms linking toxicant/injury-induced neuroinflammation to neurological outcomes.
Purpose of the Study:
- To review the interaction between the immune system and toxicant/injury-induced gliosis.
- To highlight the role of occupational injuries (e.g., TBI) and toxicants (VOCs, metals, nanomaterials) in neuroinflammation.
- To summarize recent advancements in characterizing molecular mechanisms of neuroinflammation.
Main Methods:
- Literature review focusing on toxicant and occupational injury-induced neuroinflammation.
- Analysis of signaling pathways, including protein phosphorylation and cell signaling.
- Examination of the role of reactive gliosis in CNS injury.
Main Results:
- Occupational exposures can lead to neuroinflammation, reactive gliosis, and neurological dysfunction.
- Specific toxicants and injury types (e.g., TBI) are implicated in these processes.
- Protein phosphorylation and cell signaling pathways are central to neuroinflammation development.
Conclusions:
- Further research is needed to elucidate the molecular underpinnings of toxicant- and injury-mediated neuroinflammation.
- Understanding signaling pathway interactions is critical for addressing neurodegenerative diseases.
- This review consolidates current knowledge on occupational factors contributing to neuroinflammation.
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