Summary
An omnipresent but understudied environmental risk for our immune system is pollution by nano-sized plastics. Plastic particles have been detected in a wide variety of ecosystems and are speculated to enter and spread in the food web all the way to humans. Ingested nanoplastics can translocate from the gut to the lymph and circulatory systems and have the capacity to cross the blood-brain barrier in mammals. It has been recently shown that nanoplastics cause behavioural disorders in fish, and thus may also represent a risk for human health, in particular for brain function. However, the long-term bioavailability and toxicity of nanoplastics in the brain are unknown. Microglia as the main neuroimmune cells have not only a defence function required during inflammatory conditions, but constantly sense and response to environmental changes as part of their housekeeping functions that are essential for neuronal homeostasis. This places microglia at the interface between normal and abnormal brain development and function. In line with this, we have recently discovered that chronic microglial activation causes neurodegeneration. As highly phagocytic cells, microglia internalize nanoplastics reaching the brain. This process might in turn lead to their acute or chronic activation, thereby triggering neurological disorders. In NanoGlia, we will use rodent animal models to investigate behavioural as well as cellular and molecular changes in the brain that occur upon ingestion of nanoplastics. We will further determine nanoplastics-induced developmental reprogramming events in fetal microglia that may influence brain organogenesis and function. Understanding how nanoplastics triggers microglial activation during embryogenesis and postnatal stages and whether this immune activation leads to permanent changes in brain development and function will reveal ground-breaking mechanistic insights into the environmentally triggered pathogenesis of neurological disorders.
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| Web resources: | https://cordis.europa.eu/project/id/851257 |
| Start date: | 01-04-2020 |
| End date: | 31-03-2026 |
| Total budget - Public funding: | 1 497 193,00 Euro - 1 497 193,00 Euro |
Cordis data
Original description
An omnipresent but understudied environmental risk for our immune system is pollution by nano-sized plastics. Plastic particles have been detected in a wide variety of ecosystems and are speculated to enter and spread in the food web all the way to humans. Ingested nanoplastics can translocate from the gut to the lymph and circulatory systems and have the capacity to cross the blood-brain barrier in mammals. It has been recently shown that nanoplastics cause behavioural disorders in fish, and thus may also represent a risk for human health, in particular for brain function. However, the long-term bioavailability and toxicity of nanoplastics in the brain are unknown. Microglia as the main neuroimmune cells have not only a defence function required during inflammatory conditions, but constantly sense and response to environmental changes as part of their housekeeping functions that are essential for neuronal homeostasis. This places microglia at the interface between normal and abnormal brain development and function. In line with this, we have recently discovered that chronic microglial activation causes neurodegeneration. As highly phagocytic cells, microglia internalize nanoplastics reaching the brain. This process might in turn lead to their acute or chronic activation, thereby triggering neurological disorders. In NanoGlia, we will use rodent animal models to investigate behavioural as well as cellular and molecular changes in the brain that occur upon ingestion of nanoplastics. We will further determine nanoplastics-induced developmental reprogramming events in fetal microglia that may influence brain organogenesis and function. Understanding how nanoplastics triggers microglial activation during embryogenesis and postnatal stages and whether this immune activation leads to permanent changes in brain development and function will reveal ground-breaking mechanistic insights into the environmentally triggered pathogenesis of neurological disorders.Status
SIGNEDCall topic
ERC-2019-STGUpdate Date
27-04-2024
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