Publication: Regulation of lentivirus neurovirulence by lipopolysaccharide conditioning: Suppression of CXCL10 in the brain by IL-10
Submitted Date
Received Date
Accepted Date
Issued Date
2010-02-01
Copyright Date
Announcement No.
Application No.
Patent No.
Valid Date
Resource Type
Edition
Resource Version
Language
File Type
No. of Pages/File Size
ISBN
ISSN
15506606
00221767
00221767
eISSN
Scopus ID
WOS ID
Pubmed ID
arXiv ID
Call No.
Other identifier(s)
2-s2.0-77949327634
Journal Title
Volume
Issue
item.page.oaire.edition
Start Page
End Page
Access Rights
Access Status
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Physical Location
Bibliographic Citation
Journal of Immunology. Vol.184, No.3 (2010), 1566-1574
Citation
Ferdinand Maingat, Serena Viappiani, Yu Zhu, Pornpun Vivithanaporn, Kristofor K. Ellestad, Janet Holden, Claudia Silva, Christopher Power (2010). Regulation of lentivirus neurovirulence by lipopolysaccharide conditioning: Suppression of CXCL10 in the brain by IL-10. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/29274.
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Regulation of lentivirus neurovirulence by lipopolysaccharide conditioning: Suppression of CXCL10 in the brain by IL-10
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
Other Contributor(s)
Series
Has Part
Abstract
Lentivirus infections including HIV and feline immunodeficiency virus (FIV) cause neurovirulence, which is largely mediated by innate immunity. To investigate the interactions between neurovirulence and repeated conditioning by innate immune activation, models of lentivirus infection were exposed to LPS. Gene expression in HIV-infected (HIV+) and control (HIV-) patient brains was compared by real time RT-PCR and immunocytochemistry. Supernatants from mock and HIV-infected monocyte-derived macrophages exposed to LPS were applied to human neurons. FIV-infected (FIV+) and control (FIV-) animals were exposed repeatedly to LPS postinfection together with concurrent neurobehavioral testing, viral load, and host gene analyses. Brains from HIV+ individuals exhibited induction of CD3ε, CXCL10, and granzyme A expression (p < 0.05). Supernatants from HIV+ monocyte-derived macrophages induced CXCL10 expression in neurons, which was diminished by IL-10 treatment (p < 0.05). LPS-exposed FIV+ animals demonstrated lower plasma and brain viral loads (p < 0.05). Neuronal CXCL10 expression was increased in FIV+ animals but was suppressed by LPS exposure, together with reduced brain CD3ε and granzyme A expression (p < 0.05). In conjunction with preserved NeuN-positive neuronal counts in parietal cortex (p < 0.05), FIV+ animals exposed to LPS also showed less severe neurobehavioral deficits (p < 0.05). Repeated LPS exposures suppressed CXCL10 in the brain and ensuing T cell infiltration with a concomitant reduction in neurovirulence. Thus, innate immune chronic conditioning exerted beneficial effects on neurovirulence through suppression of a specific chemotactic factor, CXCL10, mediated by IL-10, leading to reduced leukocyte infiltration and release of neurotoxic factors. Copyright © 2010 by The American Association of Immunologists, Inc.