| First Author | Rodriguez AE | Year | 2019 |
| Journal | PLoS One | Volume | 14 |
| Issue | 2 | Pages | e0212236 |
| PubMed ID | 30794604 | Mgi Jnum | J:271835 |
| Mgi Id | MGI:6282209 | Doi | 10.1371/journal.pone.0212236 |
| Citation | Rodriguez AE, et al. (2019) Enhanced IL-1beta production is mediated by a TLR2-MYD88-NLRP3 signaling axis during coinfection with influenza A virus and Streptococcus pneumoniae. PLoS One 14(2):e0212236 |
| abstractText | Viral-bacterial coinfections, such as with influenza A virus and Streptococcus pneumoniae (S.p.), are known to cause severe pneumonia. It is well known that the host response has an important role in disease. Interleukin-1beta (IL-1beta) is an important immune signaling cytokine responsible for inflammation and has been previously shown to contribute to disease severity in numerous infections. Other studies in mice indicate that IL-1beta levels are dramatically elevated during IAV-S.p. coinfection. However, the regulation of IL-1beta during coinfection is unknown. Here, we report the NLRP3 inflammasome is the major inflammasome regulating IL-1beta activation during coinfection. Furthermore, elevated IL-1beta mRNA expression is due to enhanced TLR2-MYD88 signaling, which increases the amount of pro-IL-1beta substrate for the inflammasome to process. Finally, NLRP3 and high IL-1beta levels were associated with increased bacterial load in the brain. Our results show the NLRP3 inflammasome is not protective during IAV-S.p. coinfection. |
