Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-6-11
pubmed:abstractText
Hyperthermic stress induces reactivation of herpes simplex virus type 1 (HSV-1) in latently infected mice and also stimulates corticosterone release from the adrenals via activation of the hypothalamic pituitary adrenal axis. In the present study, we tested the hypothesis that stress-induced elevation of corticosterone potentiates HSV-1 reactivation in latently infected mice. Because of the putative role of IL-6 in facilitating HSV-1 reactivation in mice, the effect of hyperthermic stress and cyanoketone treatment on IL-6 expression in the trigeminal ganglion was also measured. Preadministration of cyanoketone, a glucocorticoid synthesis inhibitor, blocked the stress-induced elevation of corticosterone in a dose-dependent manner. Furthermore, inhibition of corticosterone synthesis was correlated with reduced levels of HSV-1 reactivation in latently infected mice. Hyperthermic stress elicited a transient rise in IL-6 mRNA levels in the trigeminal ganglion, but not other cytokine transcripts investigated. In addition, there was a significant reduction in MAC-3+, CD8+, and DX5+ (NK cell marker) cells in the trigeminal ganglion of latent HSV-1-infected mice 24 h after stress. Cyanoketone blocked the stress-induced rise in IL-6 mRNA and protein expression in the trigeminal ganglion latently infected with HSV-1. Collectively, the results indicate that the activation of the hypothalamic pituitary adrenal axis plays an important role in stimulating IL-6 expression and HSV-1 reactivation in the trigeminal ganglion following hyperthermic stress of mice.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5441-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9605146-Animals, pubmed-meshheading:9605146-Antigens, CD8, pubmed-meshheading:9605146-Antigens, Differentiation, pubmed-meshheading:9605146-Corticosterone, pubmed-meshheading:9605146-Cyanoketone, pubmed-meshheading:9605146-Female, pubmed-meshheading:9605146-Herpes Simplex, pubmed-meshheading:9605146-Herpesvirus 1, Human, pubmed-meshheading:9605146-Hyperthermia, Induced, pubmed-meshheading:9605146-Hypothalamo-Hypophyseal System, pubmed-meshheading:9605146-Interleukin-6, pubmed-meshheading:9605146-Killer Cells, Natural, pubmed-meshheading:9605146-Macrophages, pubmed-meshheading:9605146-Mice, pubmed-meshheading:9605146-Mice, Inbred Strains, pubmed-meshheading:9605146-Pituitary-Adrenal System, pubmed-meshheading:9605146-RNA, Messenger, pubmed-meshheading:9605146-Stress, Physiological, pubmed-meshheading:9605146-Transcription, Genetic, pubmed-meshheading:9605146-Trigeminal Ganglion, pubmed-meshheading:9605146-Virus Activation, pubmed-meshheading:9605146-Virus Latency
pubmed:year
1998
pubmed:articleTitle
Role of the hypothalamic pituitary adrenal axis and IL-6 in stress-induced reactivation of latent herpes simplex virus type 1.
pubmed:affiliation
Department of Microbiology, Immunology, and Parasitology, Louisiana State University Medical Center, New Orleans 70112, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.