Hematopoietic cell activation in the subventricular zone after Theiler's virus infection

doi:10.1186/1742-2094-5-44

Journal of Neuroinflammation

Volume 5

Viewing options:

Abstract
Full text
PDF (6.6MB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Goings GE
Greisman A
James RE
Abram LK
Begolka WS
Miller SD
Szele FG

on PubMed

Goings GE
Greisman A
James RE
Abram LK
Begolka WS
Miller SD
Szele FG
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Research

Hematopoietic cell activation in the subventricular zone after Theiler's virus infection

Gwendolyn E Goings²^,3^,4^,5 , Adriana Greisman²^,3^,4^,5 , Rachel E James¹ , Leanne KF Abram¹ , Wendy Smith Begolka⁴^,5 , Stephen D Miller⁴^,5 and Francis G Szele¹^,2^,3

¹Department of Physiology, Anatomy, and Genetics, Oxford University, UK

²Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA

³Program in Neurobiology, Children's Memorial Research Center, Children's Memorial Hospital, Chicago, IL, USA

⁴Department of Microbiology and Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA

⁵Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA

author email corresponding author email

Journal of Neuroinflammation 2008, 5:44doi:10.1186/1742-2094-5-44


Published:	15 October 2008

Abstract

Background

The periventricular subventricular zone (SVZ) contains stem cells and is an area of active neurogenesis and migration. Since inflammation can reduce neurogenesis, we tested whether Theiler's murine encephalomyelitis virus (TMEV) induces inflammation and reduces neurogenesis in the SVZ.

Methods

We performed immmunohistochemistry for the hematopoietic cell marker CD45 throughout the central nervous system and then examined neuroblasts in the SVZ.

Results

CD45+ activation (inflammation) occurred early in the forebrain and preceded cerebellar and spinal cord inflammation. Inflammation in the brain was regionally stochastic except for the SVZ and surrounding periventricular regions where it was remarkably pronounced and consistent. In preclinical mice, SVZ neuroblasts emigrated into inflamed periventricular regions. The number of proliferating phoshpohistone3+ cells and Doublecortin+ (Dcx) SVZ neuroblasts was overall unaffected during the periods of greatest inflammation. However the number of Dcx+ and polysialylated neural cell adhesion molecule (PSA-NCAM+) SVZ neuroblasts decreased only after periventricular inflammation abated.

Conclusion

Our results suggest that after TMEV infection, the SVZ may mount an attempt at neuronal repair via emigration, a process dampened by decreases in neuroblast numbers.