Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1996-12-27
pubmed:abstractText
Superantigen hyperactivation of the immune system has variable, sometimes lethal consequences for the host. Here we show that concurrent influenza infection enhanced the effects of the bacterial superantigen staphylococcal enterotoxin B (SEB) in mice. The effect was T cell-dependent, and maximal synergism was observed when SEB was administered 7 days after the virus, a timepoint during infection associated with high viral titers, a vigorous cytotoxic T cell response, and extensive lung pathology. The influenza infection enhanced the SEB-induced cytokine response in terms of higher absolute levels of cytokine, sustained secretion, and localization to the respiratory tract. In particular, TNF and IFN-gamma were implicated in the mechanism of death because their neutralization protected the mice from death, and recombinant IFN-gamma and TNFalpha mimicked the lethal effect of SEB in influenza-infected mice. This lethal synergism between concurrent influenza infection and superantigen exposure points to the danger of secondary bacterial involvement in viral pneumonia, and suggests mechanisms that may contribute to sudden and unexpected death from influenza infection. In addition, these data demonstrate that the in vivo effects of superantigen exposure can be strongly influenced by the immune activation status of the host.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
157
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5049-60
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Lethal synergism between influenza infection and staphylococcal enterotoxin B in mice.
pubmed:affiliation
Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't