Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published online as doi:10.1189/jlb.0208108 on June 3, 2008

Published online before print June 3, 2008
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.0208108v1
84/4/932    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Google Scholar
Right arrow Articles by Dilger, R. N.
Right arrow Articles by Johnson, R. W.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dilger, R. N.
Right arrow Articles by Johnson, R. W.
(Journal of Leukocyte Biology. 2008;84:932-939.)
© 2008 by Society for Leukocyte Biology

Aging, microglial cell priming, and the discordant central inflammatory response to signals from the peripheral immune system

Ryan N. Dilger and Rodney W. Johnson1

Integrative Immunology and Behavior Program, and Department of Animal Sciences, University of Illinois, Urbana, Illinois, USA

1 Correspondence: 4 Animal Sciences Laboratory, 1207 West Gregory Dr., University of Illinois, Urbana, IL 61801, USA. E-mail: rwjohn{at}uiuc.edu

ABSTRACT

Recent studies suggest that activation of the peripheral immune system elicits a discordant central (i.e., in the brain) inflammatory response in aged but otherwise healthy subjects compared with younger cohorts. A fundamental difference in the reactive state of microglial cells in the aged brain has been suggested as the basis for this discordant inflammatory response. Thus, the aging process appears to serve as a "priming" stimulus for microglia, and upon secondary stimulation with a triggering stimulus (i.e., peripheral signals communicating infection), these primed microglia release excessive quantities of proinflammatory cytokines. Subsequently, this exaggerated cytokine release elicits exaggerated behavioral changes including anorexia, hypersomnia, lethargy, decreased social interaction, and deficits in cognitive and motor function (collectively known as the sickness behavior syndrome). Whereas this reorganization of host priorities is normally adaptive in young subjects, there is a propensity for this response to be maladaptive in aged subjects, resulting in greater severity and duration of the sickness behavior syndrome. Consequently, acute bouts of cognitive impairment in elderly subjects increase the likelihood of poor self-care behaviors (i.e., anorexia, weight loss, noncompliance), which ultimately leads to higher rates of hospitalization and mortality.

Key Words: cytokine • inflammationmicrogliasickness behavior







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the Society for Leukocyte Biology.