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The Intracellular Sensor NLRP3 Mediates Key Innate and Healing Responses to Influenza A Virus via the Regulation of Caspase-1
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SUMMARY Virus-induced IL-1β and IL-18 production in macrophages is mediated via a caspase-1 pathway. Multiple microbial components, including viral RNA, are thought to trigger assembly of the cryopyrin inflammasome and consequent caspase-1 activation. Here we demonstrate that cryopyrin−/− and caspase-1−/− mice are more susceptible than wildtype controls following infection with a pathogenic influenza A virus. This profile of enhanced morbidity correlates with decreased neutrophil and monocyte recruitment and reduced cytokine and chemokine production. Despite the effect on innate immunity, cryopyrin-deficiency was not associated with any obvious defect in virus control or on the later emergence of the adaptive response. Early epithelial necrosis was, however, more severe in the infected mutants, with extensive collagen deposition leading to later respiratory compromise. These findings reveal a novel function of the cryopyrin inflammasome in healing responses. Cryopyrin and caspase-1 are clearly central to both innate immunity and to moderating lung pathology in influenza pneumonia.
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Metadata
- Authors
- Thomas, P. G., Dash, P., Aldridge, J. R., Ellebedy, A. H., Reynolds, C., Funk, A. J., Martin, W. J., Lamkanfi, M., Webby, R. J., Boyd, K. L., Doherty, P. C., & Kanneganti, T.-D.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 30
- Issue
- 4
- Pages
- 566-575
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W1975296966
- Cited by
- 746
- References
- 15
- FWCI
- 23.16
- Type
- journal article
- Language
- en
- Open access
- bronze
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