Inflammation in the CNS and its contribution to Neurological Disease
The inflammatory response evolved to protect organisms against injury and infection. Following an injury or infection a complex cascade of events leads to the delivery of blood-borne leucocytes to sites of injury to kill potential pathogens and promote tissue repair. However, the powerful inflammatory response has the capacity to cause damage to normal tissue and dysregulation of the innate or acquired immune response is involved in different pathologies. It has long been known that Multiple Sclerosis is an inflammatory disease of the brain but it is now recognized that inflammation may contribute to diseases such as stroke, traumatic brain injury, HIV-related dementia, Alzheimer's disease and prion disease. The recognition of an inflammatory component in the pathology of these different diseases has come from the development of new techniques and reagents for the study of inflammation biology in brain pathology. It is now known that the resident macrophages of the central nervous system (CNS), the microglia, may exist in many different states of activation and contribute to the outcome of neurological disease in diverse ways. The goal of my research group the CNS Inflammation Group is to discover how inflammation contributes to the outcome of neurological disease. This information may help in the development of therapies to treat acute and chronic neurodegenerative conditions, which at present are largely untreated.
Inflammation biology in the brain is a complex subject and requires expertise in many different areas. We have collaborations with academic laboratories across the University of Southampton, the UK, as well as with laboratories across Europe.
Affiliate research group(s)
Institute for Life Sciences (IfLS), Southampton Neuroscience Group (SoNG)
In this project we are investigating whether systemic infections can contribute to driving the progression of the progressive phase of multiple sclerosis.
Using novel cell-labelling techniques and functionalised nanoparticles, we track macrophages and T cell recruitment to the brain and assess the role of cell mediated and humoral immunity in the initiation and/or progression of CNS inflammation.
Using immunocytochemistry, molecular biology and formal behavioural testing techniques we investigate the biological nature of immune-to-brain communication elicited by immune-mediated lung disease.
We are investigating the microglia activation in a model of prion disease, mouse scrapie.
Using immunocytochemistry, molecular biology and formal behavioural testing techniques we investigate antibody-mediated neuronal damage in lupus.
Using immunocytochemistry, cell biology, imaging and formal behavioural testing techniques we investigate how systemic infections impact on the brain.
Using novel models for AMD, we will investigate the functional role of antibodies in disease onset and progression.
Oligodendrocyte progenitor cells (OPCs) may be altered in Alzheimer’s disease.
Can Wlds protect against axonal dysfunction and degeneration in a transgenic model of Alzheimer’s disease?
Professor V Hugh Perry
Centre for Biological Sciences Mailpoint 840 (room LD80b) Level D Laboratories and Pathology Block Southampton General Hospital Tremona Road Southampton SO16 6YD Phone: 023-8120-6103
Room Number: SGH/LD840