Genomic Profiling of Tumor Necrosis Factor Alpha (TNF-α) Receptor and Interleukin-1 Receptor Knockout Mice Reveals a Link between TNF-α Signaling and Increased Severity of 1918 Pandemic Influenza Virus Infection▿ †
Identifieur interne : 003207 ( Main/Exploration ); précédent : 003206; suivant : 003208Genomic Profiling of Tumor Necrosis Factor Alpha (TNF-α) Receptor and Interleukin-1 Receptor Knockout Mice Reveals a Link between TNF-α Signaling and Increased Severity of 1918 Pandemic Influenza Virus Infection▿ †
Auteurs : Sarah E. Belisle ; Jennifer R. Tisoncik ; Marcus J. Korth ; Victoria S. Carter ; Sean C. Proll ; David E. Swayne ; Mary Pantin-Jackwood ; Terrence M. Tumpey ; Michael G. KatzeSource :
- Journal of Virology [ 0022-538X ] ; 2010.
Descripteurs français
- KwdFr :
- ARN messager (génétique), Analyse de profil d'expression de gènes, Animaux, Cellules dendritiques (métabolisme), Cellules dendritiques (virologie), Communication cellulaire, Facteur de nécrose tumorale alpha (physiologie), Infections à Orthomyxoviridae (virologie), Marqueurs biologiques (métabolisme), Mouvement cellulaire, Pandémies, RT-PCR, Récepteur au facteur de nécrose tumorale de type I (génétique), Récepteur à l'interleukine-1 de type I (génétique), Souris, Souris de lignée C57BL, Souris knockout, Séquençage par oligonucléotides en batterie, Technique de Western, Transduction du signal (physiologie), Triazoles, Virus de la grippe A (pathogénicité).
- MESH :
- génétique : ARN messager, Récepteur au facteur de nécrose tumorale de type I, Récepteur à l'interleukine-1 de type I.
- métabolisme : Cellules dendritiques, Marqueurs biologiques.
- pathogénicité : Virus de la grippe A.
- physiologie : Facteur de nécrose tumorale alpha, Transduction du signal.
- virologie : Cellules dendritiques, Infections à Orthomyxoviridae.
- Analyse de profil d'expression de gènes, Animaux, Communication cellulaire, Mouvement cellulaire, Pandémies, RT-PCR, Souris, Souris de lignée C57BL, Souris knockout, Séquençage par oligonucléotides en batterie, Technique de Western, Triazoles.
English descriptors
- KwdEn :
- Animals, Biomarkers (metabolism), Blotting, Western, Cell Communication, Cell Movement, Dendritic Cells (metabolism), Dendritic Cells (virology), Gene Expression Profiling, Influenza A virus (pathogenicity), Mice, Mice, Inbred C57BL, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Orthomyxoviridae Infections (virology), Pandemics, RNA, Messenger (genetics), Receptors, Interleukin-1 Type I (genetics), Receptors, Tumor Necrosis Factor, Type I (genetics), Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction (physiology), Triazoles, Tumor Necrosis Factor-alpha (physiology).
- MESH :
- chemical , genetics : RNA, Messenger, Receptors, Interleukin-1 Type I, Receptors, Tumor Necrosis Factor, Type I.
- chemical , metabolism : Biomarkers.
- metabolism : Dendritic Cells.
- pathogenicity : Influenza A virus.
- physiology : Signal Transduction, Tumor Necrosis Factor-alpha.
- virology : Dendritic Cells, Orthomyxoviridae Infections.
- Animals, Blotting, Western, Cell Communication, Cell Movement, Gene Expression Profiling, Mice, Mice, Inbred C57BL, Mice, Knockout, Oligonucleotide Array Sequence Analysis, Pandemics, Reverse Transcriptase Polymerase Chain Reaction, Triazoles.
Abstract
The influenza pandemic of 1918 to 1919 was one of the worst global pandemics in recent history. The highly pathogenic nature of the 1918 virus is thought to be mediated in part by a dysregulation of the host response, including an exacerbated proinflammatory cytokine response. In the present study, we compared the host transcriptional response to infection with the reconstructed 1918 virus in wild-type, tumor necrosis factor (TNF) receptor-1 knockout (TNFRKO), and interleukin-1 (IL-1) receptor-1 knockout (IL1RKO) mice as a means of further understanding the role of proinflammatory cytokine signaling during the acute response to infection. Despite reported redundancy in the functions of IL-1β and TNF-α, we observed that reducing the signaling capacity of each of these molecules by genetic disruption of their key receptor genes had very different effects on the host response to infection. In TNFRKO mice, we found delayed or decreased expression of genes associated with antiviral and innate immune signaling, complement, coagulation, and negative acute-phase response. In contrast, in IL1RKO mice numerous genes were differentially expressed at 1 day postinoculation, including an increase in the expression of genes that contribute to dendritic and natural killer cell processes and cellular movement, and gene expression profiles remained relatively constant at later time points. We also observed a compensatory increase in TNF-α expression in virus-infected IL1RKO mice. Our data suggest that signaling through the IL-1 receptor is protective, whereas signaling through the TNF-α receptor increases the severity of 1918 virus infection. These findings suggest that manipulation of these pathways may have therapeutic benefit.
Url:
DOI: 10.1128/JVI.01310-10
PubMed: 20926563
PubMed Central: 3004331
Affiliations:
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Le document en format XML
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The highly pathogenic nature of the 1918 virus is thought to be mediated in part by a dysregulation of the host response, including an exacerbated proinflammatory cytokine response. In the present study, we compared the host transcriptional response to infection with the reconstructed 1918 virus in wild-type, tumor necrosis factor (TNF) receptor-1 knockout (TNFRKO), and interleukin-1 (IL-1) receptor-1 knockout (IL1RKO) mice as a means of further understanding the role of proinflammatory cytokine signaling during the acute response to infection. Despite reported redundancy in the functions of IL-1β and TNF-α, we observed that reducing the signaling capacity of each of these molecules by genetic disruption of their key receptor genes had very different effects on the host response to infection. In TNFRKO mice, we found delayed or decreased expression of genes associated with antiviral and innate immune signaling, complement, coagulation, and negative acute-phase response. In contrast, in IL1RKO mice numerous genes were differentially expressed at 1 day postinoculation, including an increase in the expression of genes that contribute to dendritic and natural killer cell processes and cellular movement, and gene expression profiles remained relatively constant at later time points. We also observed a compensatory increase in TNF-α expression in virus-infected IL1RKO mice. Our data suggest that signaling through the IL-1 receptor is protective, whereas signaling through the TNF-α receptor increases the severity of 1918 virus infection. These findings suggest that manipulation of these pathways may have therapeutic benefit.</p></div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Belisle, Sarah E" sort="Belisle, Sarah E" uniqKey="Belisle S" first="Sarah E." last="Belisle">Sarah E. Belisle</name><name sortKey="Carter, Victoria S" sort="Carter, Victoria S" uniqKey="Carter V" first="Victoria S." last="Carter">Victoria S. Carter</name><name sortKey="Katze, Michael G" sort="Katze, Michael G" uniqKey="Katze M" first="Michael G." last="Katze">Michael G. Katze</name><name sortKey="Korth, Marcus J" sort="Korth, Marcus J" uniqKey="Korth M" first="Marcus J." last="Korth">Marcus J. Korth</name><name sortKey="Pantin Jackwood, Mary" sort="Pantin Jackwood, Mary" uniqKey="Pantin Jackwood M" first="Mary" last="Pantin-Jackwood">Mary Pantin-Jackwood</name><name sortKey="Proll, Sean C" sort="Proll, Sean C" uniqKey="Proll S" first="Sean C." last="Proll">Sean C. Proll</name><name sortKey="Swayne, David E" sort="Swayne, David E" uniqKey="Swayne D" first="David E." last="Swayne">David E. Swayne</name><name sortKey="Tisoncik, Jennifer R" sort="Tisoncik, Jennifer R" uniqKey="Tisoncik J" first="Jennifer R." last="Tisoncik">Jennifer R. Tisoncik</name><name sortKey="Tumpey, Terrence M" sort="Tumpey, Terrence M" uniqKey="Tumpey T" first="Terrence M." last="Tumpey">Terrence M. 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