Linked Life Data

17703413

Source:http://linkedlifedata.com/resource/pubmed/id/17703413

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-8-17
pubmed:abstractText
The innate immune system mounts the first host response to pathogens. Because alpha-defensins, which are cationic antimicrobial peptides of polymorphonuclear neutrophils and other leukocytes, are important effectors of the innate immune system, we studied the antiviral activity of human alpha-defensin-1 (also known as "human neutrophil peptide-1" [HNP-1]) against influenza virus in vitro. Treatment of cell cultures with HNP-1 soon after infection resulted in marked inhibition of influenza virus replication and viral protein synthesis. This effect was not due to cytotoxicity or to a direct effect on the virus. Treatment of cells with HNP-1 followed by its removal before infection also inhibited viral replication, suggesting that the inhibition was due to the modulation of cellular pathways. HNP-1 treatment inhibited protein kinase C (PKC) activation in infected cells, suggesting the involvement of the PKC pathway. Our data expand the previously known activity of alpha -defensins against influenza virus. Characterizing the mechanism of action of alpha -defensins may lead to the identification of new strategies for prevention and therapy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1899
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
196
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
835-43
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
alpha-Defensin inhibits influenza virus replication by cell-mediated mechanism(s).
pubmed:affiliation
Division of Infectious Diseases, Mount Sinai School of Medicine, New York, NY 100129, USA. Mirella.Salvatore@mssm.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural