Article ; Online: Mice lacking both TNF and IL-1 receptors exhibit reduced lung inflammation and delay in onset of death following infection with a highly virulent H5N1 virus.
The Journal of infectious diseases
2010 Volume 202, Issue 8, Page(s) 1161–1170
Abstract: ... receptors, TNF-R1, TNF-R2, and IL-1-RI.: Results: Triple mutant mice exhibited reduced morbidity and ... such differences were observed with the less virulent A/PR/8/34 (H1N1) virus. H5N1-infected triple mutant mice ... Conclusions: The combined signaling from the TNF or IL-1 receptors promotes maximal lung inflammation ...
| Abstract | Background: Highly pathogenic avian influenza viruses of the H5N1 subtype continue to cross the species barrier to infect humans and cause severe disease. It has been suggested that an exaggerated immune response contributes to the pathogenesis of H5N1 virus infection in mammals. In particular, H5N1 virus infections are associated with a high expression of the proinflammatory cytokines, including interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α). Methods: We investigated the compounding affects of both cytokines on the outcome of H5N1 virus disease by using triple mutant mice deficient in 3 signaling receptors, TNF-R1, TNF-R2, and IL-1-RI. Results: Triple mutant mice exhibited reduced morbidity and a significant delay in mortality following lethal challenge with a lethal H5N1 virus, whereas no such differences were observed with the less virulent A/PR/8/34 (H1N1) virus. H5N1-infected triple mutant mice displayed diminished cytokine production in lung tissue and a quantifiable decrease of macrophages and neutrophils in the lungs postinfection. Moreover, morphometric analysis of airway sections revealed less extensive inflammation in H5N1-infected triple mutant mice, compared with infected wild-type mice. Conclusions: The combined signaling from the TNF or IL-1 receptors promotes maximal lung inflammation that may contribute to the severity of disease caused by H5N1 virus infection. |
||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|
| MeSH term(s) | Animals ; Brain/virology ; Cell Count ; Cytokines/deficiency ; Cytokines/immunology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/mortality ; Influenza A Virus, H5N1 Subtype ; Lung Diseases/genetics ; Lung Diseases/immunology ; Lung Diseases/mortality ; Lung Diseases/physiopathology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mutation/genetics ; Neutrophils/immunology ; Orthomyxoviridae Infections/genetics ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/mortality ; Orthomyxoviridae Infections/physiopathology ; Receptors, Interleukin-1/genetics ; Receptors, Tumor Necrosis Factor/genetics ; Signal Transduction ; Viral Load | ||||||||||
| Chemical Substances | Cytokines ; Receptors, Interleukin-1 ; Receptors, Tumor Necrosis Factor | ||||||||||
| Language | English | ||||||||||
| Publishing date | 2010-09-14 | ||||||||||
| Publishing country | United States | ||||||||||
| Document type | Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. | ||||||||||
| ZDB-ID | 3019-3 | ||||||||||
| ISSN | 1537-6613 ; 0022-1899 | ||||||||||
| ISSN (online) | 1537-6613 | ||||||||||
| ISSN | 0022-1899 | ||||||||||
| DOI | 10.1086/656365 | ||||||||||
| Shelf mark |
|
||||||||||
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
More links
Kategorien
In stock of ZB MED Cologne/Königswinter
| Uh II Zs.50: Show issues | Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG) |
|||
| Zs.MO 445: Show issues |
Order via subito
This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.