Role of microglia and astrocytes in the process of neuroinflammation

Microglial activation represents an increasingly important concept in the pathogenesis of neurodegenerative disorders such as Alzheimer and Parkinson disease, as well as in stroke, traumatic brain injury, demyelinating conditions and pathology associated with CNS infections. There is a tight regulatory environment of the brain and a balance between inflammation-induced tissue repair and tissue damage. The major resident inflammatory cells in the CNS are microglia. These cells are especially important to guard the integrity and homeostasis of the brain. In normal conditions they are quiescent cells, but become activated by injury or infection and have been suggested to represent the first line of defence for the CNS. However, when the state of glia activation is becoming chronic than activated microglia release various pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), chemokines (IL-8, MIP-1α, MIP-1β, MCP-1), proteases, as well as oxidative and nitrosative free radicals (superoxide, nitric oxide, peroxynitrite) leading to the neuronal cell death. On the other hand microglia can produce also anti-inflammatory mediators, such as TGF-β, PGE2 and IL-1 receptor antagonist (IL-1ra) and due to their ability of phagocytosis microglia can also play the role of scavengers. Astrocytes are not commonly associated with immunological reactions, and it is well accepted that their role in CNS immunity is largely regulatory. In this chapter the role or microglia and astrocytes in the neuroinflammation involved in the various CNS pathologies is discussed including the characterization the inflammatory mediators and the mechanisms of inflammatory-induced neuronal cell death.

PRICE Anna;  KINSNER-OVASKAINEN Agnieszka; 

2013-12-19

Nova Science Publishers, Inc.

JRC73731

978-1-62618-448-0,   

https://www.novapublishers.com/catalog/product_info.php?products_id=40547,    https://publications.jrc.ec.europa.eu/repository/handle/JRC73731,