Microglia Play a Major Role in Direct Viral-Induced Demyelination
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 C...
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Published in | Clinical & developmental immunology Vol. 2013; no. 2013; pp. 1 - 12 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
01.01.2013
Wiley |
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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. |
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AbstractList | 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. 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. |
Author | Ramachandra, S. G. Chatterjee, Dhriti Das Sarma, Jayasri Biswas, Kaushiki Nag, Soma |
AuthorAffiliation | 1 Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata (IISER-K), Mohanpur Campus, P.O. Box BCKV Campus Main Office, Nadia, West Bengal Mohanpur 741252, India 2 Central Animal Facility, Indian Institute of Science, Bangalore 560012, India |
AuthorAffiliation_xml | – name: 1 Department of Biological Sciences, Indian Institute of Science Education and Research-Kolkata (IISER-K), Mohanpur Campus, P.O. Box BCKV Campus Main Office, Nadia, West Bengal Mohanpur 741252, India – name: 2 Central Animal Facility, Indian Institute of Science, Bangalore 560012, India |
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Copyright | Copyright © 2013 Dhriti Chatterjee et al. Copyright © 2013 Dhriti Chatterjee et al. 2013 |
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SubjectTerms | Animals Calcium-Binding Proteins - genetics Calcium-Binding Proteins - immunology Central Nervous System - immunology Central Nervous System - pathology Central Nervous System - virology Demyelinating Diseases - immunology Demyelinating Diseases - pathology Demyelinating Diseases - virology Disease Models, Animal Gene Expression Humans Meningoencephalitis - immunology Meningoencephalitis - pathology Meningoencephalitis - virology Mice Mice, Inbred C57BL Microfilament Proteins - genetics Microfilament Proteins - immunology Microglia - immunology Microglia - pathology Microglia - virology Multiple Sclerosis - immunology Multiple Sclerosis - pathology Multiple Sclerosis - virology Murine hepatitis virus - immunology Myelin Sheath - immunology Myelin Sheath - pathology Myelin Sheath - virology Myelitis, Transverse - immunology Myelitis, Transverse - pathology Myelitis, Transverse - virology Spinal Cord - immunology Spinal Cord - pathology Spinal Cord - virology Tissue Culture Techniques |
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Title | Microglia Play a Major Role in Direct Viral-Induced Demyelination |
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