Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-1-10
pubmed:abstractText
The tachykinins are implicated in neurogenic inflammation and the neuropeptide substance P in particular has been shown to be a proinflammatory mediator. A role for the tachykinins in host response to viral infection has been previously demonstrated using either TAC1- or NK1 receptor-deficient transgenic mice. However, due to redundancy in the peptide-receptor complexes we wished determine whether a deficiency in TAC1 and NK1(R) in combination exhibited an enhanced phenotype. TAC1 and NK1(R)-deficient mice were therefore crossed to generate transgenic mice in both (NK1(-/-)×TAC1(-/-)). As expected, after infection with the respiratory pathogen murine gammaherpesvirus (MHV-68), TAC1 and NK1(R)-deficient mice were more susceptible to infection than wild-type C57BL/6 controls. However, unexpectedly, NK1(-/-)×TAC1(-/-) mice were more resistant to infection arguing for a lack of feedback inhibition through alternative receptors in these mice. Histopathological examination did not show any great differences in the inflammatory responses between groups of infected animals, except for the presence of focal perivascular B cell accumulations in lungs of all the knockout mice. These were most pronounced in the NK1(-/-)×TAC1(-/-) mice. These results confirm an important role for TAC1 and NK1(R) in the control of viral infection but reinforce the complex nature of the peptide-receptor interactions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1532-2785
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-53
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Altered host response to murine gammaherpesvirus 68 infection in mice lacking the tachykinin 1 gene and the receptor for substance P.
pubmed:affiliation
Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't