Linked Life Data

1654165

Source:http://linkedlifedata.com/resource/pubmed/id/1654165

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1991-10-22
pubmed:abstractText
Stressful events suppress a broad spectrum of both humoral and cellular immunological responses. However, studies of the effects of stress on the development of specific antiviral immune responses have not been reported. We have utilized an established murine model of an acute, local footpad Herpes simplex virus type 1 (HSV-1) infection to study the effect of restraint stress on the generation of HSV-specific cytotoxic T lymphocytes (CTL) and natural killer (NK) cell activity. Lymphoproliferative responses in the popliteal lymph nodes following footpad infection as well as the generation of HSV-specific CTL and NK cell activity were depressed in restrained mice compared to infected, unrestrained controls. Frequency analyses of HSV-specific pre-CTL indicated that suppression of the CTL response occurred early in the sequence of events that precedes the generation of functionally lytic CTL and was not mediated by a diminished IL-2 response. Although restrained mice exhibited fewer lymphocytes in the popliteal lymph nodes, the subset distribution was the same as that in the unrestrained controls. Furthermore, stress-induced immunosuppression resulted in a higher titer of infectious HSV at the site of infection. Overall, these findings provide evidence that physiological changes associated with restraint stress can influence the immune response to a specific viral infection and alter the course of viral pathogenesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0889-1591
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
170-92
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Stress-induced suppression of herpes simplex virus (HSV)-specific cytotoxic T lymphocyte and natural killer cell activity and enhancement of acute pathogenesis following local HSV infection.
pubmed:affiliation
Department of Medical Microbiology and Immunology, Ohio State University College of Medicine, Columbus 43210.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.