Publication: Nitric Oxide Protects against Infection-Induced Neuroinflammation by Preserving the Stability of the Blood-Brain Barrier
Submitted Date
Received Date
Accepted Date
Issued Date
2016-02
Copyright Date
Announcement No.
Application No.
Patent No.
Valid Date
Resource Type
Edition
Resource Version
Language
eng
File Type
No. of Pages/File Size
ISBN
ISSN
eISSN
DOI
Scopus ID
WOS ID
Pubmed ID
arXiv ID
Call No.
Other identifier(s)
Journal Title
Volume
Issue
item.page.oaire.edition
Start Page
End Page
Access Rights
Access Status
Rights
Rights Holder(s)
Physical Location
Bibliographic Citation
Plos One. Vol.12, No.2 (2016), e1005442
Citation
Gabriela C. Olivera, Xiaoyuan Ren, Suman K. Vodnala, Jun Lu, Lucia Coppo, Chaniya Leepiyasakulchai, Arne Holmgren, Krister Kristensson, Martin E. Rottenberg (2016). Nitric Oxide Protects against Infection-Induced Neuroinflammation by Preserving the Stability of the Blood-Brain Barrier. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/2134.
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Nitric Oxide Protects against Infection-Induced Neuroinflammation by Preserving the Stability of the Blood-Brain Barrier
Alternative Title(s)
Author's Affiliation
Author's E-mail
Editor(s)
Editor's Affiliation
Corresponding Author(s)
Creator(s)
Compiler
Advisor(s)
Illustrator(s)
Applicant(s)
Inventor(s)
Issuer
Assignee
Series
Has Part
Abstract
Nitric oxide (NO) generated by inducible NO synthase (iNOS) is critical for defense against intracellular pathogens but may mediate inflammatory tissue damage. To elucidate the role of iNOS in neuroinflammation, infections with encephalitogenic Trypanosoma brucei parasites were compared in inos-/- and wild-type mice. Inos-/- mice showed enhanced brain invasion by parasites and T cells, and elevated protein permeability of cerebral vessels, but similar parasitemia levels. Trypanosome infection stimulated T cell- and TNF-mediated iNOS expression in perivascular macrophages. NO nitrosylated and inactivated pro-inflammatory molecules such as NF-κΒp65, and reduced TNF expression and signalling. iNOS-derived NO hampered both TNF- and T cell-mediated parasite brain invasion. In inos-/- mice, TNF stimulated MMP, including MMP9 activity that increased cerebral vessel permeability. Thus, iNOS-generated NO by perivascular macrophages, strategically located at sites of leukocyte brain penetration, can serve as a negative feed-back regulator that prevents unlimited influx of inflammatory cells by restoring the integrity of the blood-brain barrier.