Breaking Bad: Inflammasome Activation by Respiratory Viruses
The nucleotide-binding domain leucine-rich repeat-containing receptor (NLR) family is a group of intracellular sensors activated in response to harmful stimuli, such as invading pathogens. Some NLR family members form large multiprotein complexes known as inflammasomes, acting as a platform for acti...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-07-01
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| Series: | Biology |
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| Online Access: | https://www.mdpi.com/2079-7737/12/7/943 |
| _version_ | 1797590249333850112 |
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| author | Julia A. Cerato Emanuelle F. da Silva Barbara N. Porto |
| author_facet | Julia A. Cerato Emanuelle F. da Silva Barbara N. Porto |
| author_sort | Julia A. Cerato |
| collection | DOAJ |
| description | The nucleotide-binding domain leucine-rich repeat-containing receptor (NLR) family is a group of intracellular sensors activated in response to harmful stimuli, such as invading pathogens. Some NLR family members form large multiprotein complexes known as inflammasomes, acting as a platform for activating the caspase-1-induced canonical inflammatory pathway. The canonical inflammasome pathway triggers the secretion of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 by the rapid rupture of the plasma cell membrane, subsequently causing an inflammatory cell death program known as pyroptosis, thereby halting viral replication and removing infected cells. Recent studies have highlighted the importance of inflammasome activation in the response against respiratory viral infections, such as influenza and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While inflammasome activity can contribute to the resolution of respiratory virus infections, dysregulated inflammasome activity can also exacerbate immunopathology, leading to tissue damage and hyperinflammation. In this review, we summarize how different respiratory viruses trigger inflammasome pathways and what harmful effects the inflammasome exerts along with its antiviral immune response during viral infection in the lungs. By understanding the crosstalk between invading pathogens and inflammasome regulation, new therapeutic strategies can be exploited to improve the outcomes of respiratory viral infections. |
| first_indexed | 2024-03-11T01:17:52Z |
| format | Article |
| id | doaj.art-a5408e9d999541148566d782387b1e20 |
| institution | Directory Open Access Journal |
| issn | 2079-7737 |
| language | English |
| last_indexed | 2024-03-11T01:17:52Z |
| publishDate | 2023-07-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biology |
| spelling | doaj.art-a5408e9d999541148566d782387b1e202023-11-18T18:23:23ZengMDPI AGBiology2079-77372023-07-0112794310.3390/biology12070943Breaking Bad: Inflammasome Activation by Respiratory VirusesJulia A. Cerato0Emanuelle F. da Silva1Barbara N. Porto2Department of Medical Microbiology and Infectious Diseases, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaDepartment of Medical Microbiology and Infectious Diseases, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaDepartment of Medical Microbiology and Infectious Diseases, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB R3E 0J9, CanadaThe nucleotide-binding domain leucine-rich repeat-containing receptor (NLR) family is a group of intracellular sensors activated in response to harmful stimuli, such as invading pathogens. Some NLR family members form large multiprotein complexes known as inflammasomes, acting as a platform for activating the caspase-1-induced canonical inflammatory pathway. The canonical inflammasome pathway triggers the secretion of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 by the rapid rupture of the plasma cell membrane, subsequently causing an inflammatory cell death program known as pyroptosis, thereby halting viral replication and removing infected cells. Recent studies have highlighted the importance of inflammasome activation in the response against respiratory viral infections, such as influenza and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While inflammasome activity can contribute to the resolution of respiratory virus infections, dysregulated inflammasome activity can also exacerbate immunopathology, leading to tissue damage and hyperinflammation. In this review, we summarize how different respiratory viruses trigger inflammasome pathways and what harmful effects the inflammasome exerts along with its antiviral immune response during viral infection in the lungs. By understanding the crosstalk between invading pathogens and inflammasome regulation, new therapeutic strategies can be exploited to improve the outcomes of respiratory viral infections.https://www.mdpi.com/2079-7737/12/7/943respiratory virusinflammasomevirus infectionantiviral responsedisease pathogenesis |
| spellingShingle | Julia A. Cerato Emanuelle F. da Silva Barbara N. Porto Breaking Bad: Inflammasome Activation by Respiratory Viruses Biology respiratory virus inflammasome virus infection antiviral response disease pathogenesis |
| title | Breaking Bad: Inflammasome Activation by Respiratory Viruses |
| title_full | Breaking Bad: Inflammasome Activation by Respiratory Viruses |
| title_fullStr | Breaking Bad: Inflammasome Activation by Respiratory Viruses |
| title_full_unstemmed | Breaking Bad: Inflammasome Activation by Respiratory Viruses |
| title_short | Breaking Bad: Inflammasome Activation by Respiratory Viruses |
| title_sort | breaking bad inflammasome activation by respiratory viruses |
| topic | respiratory virus inflammasome virus infection antiviral response disease pathogenesis |
| url | https://www.mdpi.com/2079-7737/12/7/943 |
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