Characterisation of microglia after an acute brain injury
Research type
Research Study
Full title
Characterisation of microglia after an acute brain injury
IRAS ID
200267
Contact name
Fiona Calvert
Contact email
Sponsor organisation
Cambridge University Hospitals NHS Foundation Trust and the University of Cambridge
Duration of Study in the UK
3 years, 0 months, 1 days
Research summary
Acute brain injury (ABI) is usually followed by a severe inflammatory response that can causes even more damage to a patient. This inflammation has a range of consequences: oedema (swelling), hypoxia (lack of oxygen), ischaemia (interruption in the blood supply) and ultimately neuron (nerve) loss. Better treatments to control inflammation following ABI could have a major positive impact on patient survival and recovery.
In the brain the cells that control inflammation are called a type of white blood cell called microglia. Microglia are located throughout the brain and spinal cord and account for 10–15% of all cells found within the brain. As the resident white blood cells, they are the main active immune defence in the central nervous system (CNS). Microglia are part of an important class of cells known as macrophages that have two main states: M1 and M2. M1 cells are pro-inflammatory, leading to more inflammation, while M2 are anti-inflammatory, and drive wound healing. Reducing the number of pro-inflammatory (M1) microglia prevents white brain matter injury, reduces nerve cell loss and improves neurological recovery. However, human microglia are a very challenging cell to study because they are hard to access. As a result, there is very little known about what controls the shift between M1 and M2 microglia,
In this study we aim to investigate what determines whether microglia develop into an M1 or M2 phenotype. Brain and skin biopsys will be collected from patients who have suffered an acute brain injury. Microglia and cell lines will be grown in the laboratory to try to determine the cellular and genetic mechanisms that drive pro-inflammatory and pro-repair microglia. The identification of cell signalling pathways driving the human microglia response will be novel and may unveil potential therapeutic targets.
REC name
London - Bromley Research Ethics Committee
REC reference
16/LO/2168
Date of REC Opinion
3 Mar 2017
REC opinion
Further Information Favourable Opinion