| First Author | Zhang T | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 513 |
| Issue | 3 | Pages | 675-680 |
| PubMed ID | 30982580 | Mgi Jnum | J:290395 |
| Mgi Id | MGI:6442808 | Doi | 10.1016/j.bbrc.2019.04.004 |
| Citation | Zhang T, et al. (2019) NLRP3/ASC/Caspase-1 axis and serine protease activity are involved in neutrophil IL-1beta processing during Streptococcus pneumoniae infection. Biochem Biophys Res Commun 513(3):675-680 |
| abstractText | Streptococcus pneumoniae is a pathogenic bacterium that can cause severe invasive diseases, such as pneumonia, otitis media and meningitis. The pro-inflammatory cytokine, IL-1beta, has been reported to play important role in host defense against S. pneumoniae. The mechanism of IL-1beta maturation and secretion in macrophages has been well studied. However, the precise mechanism of IL-1beta processing within neutrophils upon S. pneumoniae infection remains unclear. In this study, mouse peritoneal neutrophils from C57BL/6 WT and inflammasome components knockout mice were infected by S. pneumoniae in vitro. The results showed that NLRP3 inflammasome is critically involved in neutrophil IL-1beta secretion, while the AIM2 and NLRC4 inflammasomes were dispensable. Moreover, the upstream kinase, JNK, modulates ASC oligomerization and consequent caspase-1 activation and IL-1beta secretion. Additionally, neutrophil serine proteases also participate in IL-1beta secretion by mediating ASC oligomerization and caspase-1 activation. Taken together, these findings indicated that both the NLRP3 inflammasome-related pathway and neutrophil serine protease mediate IL-1beta processing upon S. pneumoniae infection. |
