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| Funder | Swedish Research Council |
|---|---|
| Recipient Organization | Karolinska Institutet |
| Country | Sweden |
| Start Date | Jan 01, 2021 |
| End Date | Dec 31, 2024 |
| Duration | 1,460 days |
| Number of Grantees | 1 |
| Roles | Principal Investigator |
| Data Source | Swedish Research Council |
| Grant ID | 2020-02061_VR |
Bacterial meningitis is caused by bacteria that from the blood penetrate the blood-brain barrier (BBB) and invade the.
Streptococcus pneumoniae (the pneumococcus) is the major cause of bacterial meningitis worldwide. 50-70% among survivors suffer from brain damages, such as cognitive disorders, hearing loss, or other neurological deficiencies, and neuronal cell damage is often the reason of these brain sequelae. How pneumococci cause neuronal cell damage is still poorly understood.
Here, we want to study the biology of how pneumococci injure neurons.
By understanding how pneumococci interact with neurons and we want to block pneumococcal-neuron interaction to prevent neuronal damage.
In this way, we can protect neurons from pathogens, and can also prevent the onset of neurodegenerative disorders that are more likely to develop following bacterial meningitis. Microglia, the resident macrophages of the brain, have the primary function to kill pathogens by phagocytosis. Little is known about the interplay between S. pneumoniae and microglia.
In this project we want to study the molecular mechanism that triggers microglial uptake and phagocytosis of bacteria.
By understanding this, we then want to investigate how to enhance the capacity of microglia to quickly recognize and kill pneumococci.
Modulation of microglial responses, reinforcing the phagocytic capacity and dampening neuroinflammation, could represent great advantages in the management of bacterial meningitis.
Karolinska Institutet
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