ePrints@IIScePrints@IISc Home | About | Browse | Latest Additions | Advanced Search | Contact | Help

Microglia play a major role in direct viral-induced demyelination

Chatterjee, Dhriti and Biswas, Kaushiki and Nag, Soma and Ramachandra, SG and Das Sarma, Jayasri (2013) Microglia play a major role in direct viral-induced demyelination. In: Clinical and Developmental Immunology . 510396_1-510396_12.

[img]
Preview
PDF
Clin_Dev_Imm_510396_2013.pdf
Available under License Creative Commons Attribution.

Download (9Mb) | Preview
Official URL: http://dx.doi.org/10.1155/2013/510396

Abstract

Microglia are the resident macrophage-like populations in the central nervous system (CNS). Microglia remain quiescent, unable to perform effector and antigen presentation (APC) functions until activated by injury or infection, and have been suggested to represent the first line of defence for the CNS. Previous studies demonstrated that microglia can be persistently infected by neurotropic mouse hepatitis virus (MHV) which causes meningoencephalitis, myelitis with subsequent axonal loss, and demyelination and serve as a virus-induced model of human neurological disease multiple sclerosis (MS). Current studies revealed that MHV infection is associated with the pronounced activation of microglia during acute inflammation, as evidenced by characteristic changes in cellular morphology and increased expression of microglia-specific proteins, Iba1 (ionized calcium-binding adaptor molecule 1), which is a macrophage/microglia-specific novel calcium-binding protein and involved in membrane ruffling and phagocytosis. During chronic inflammation (day 30 postinfection), microglia were still present within areas of demyelination. Experiments performed in ex vivo spinal cord slice culture and in vitro neonatal microglial culture confirmed direct microglial infection. Our results suggest that MHV can directly infect and activate microglia during acute inflammation, which in turn during chronic inflammation stage causes phagocytosis of myelin sheath leading to chronic inflammatory demyelination.

Item Type: Journal Article
Related URLs:
Additional Information: Copyright of this article belongs to the authors
Department/Centre: Others
Date Deposited: 16 Aug 2013 09:43
Last Modified: 16 Aug 2013 09:45
URI: http://eprints.iisc.ernet.in/id/eprint/46998

Actions (login required)

View Item View Item