| First Author | Chen L | Year | 2019 |
| Journal | Mol Med Rep | Volume | 20 |
| Issue | 6 | Pages | 5345-5352 |
| PubMed ID | 31638229 | Mgi Jnum | J:298521 |
| Mgi Id | MGI:6480212 | Doi | 10.3892/mmr.2019.10752 |
| Citation | Chen L, et al. (2019) Downregulation of FSTL1 attenuates the inflammation injury during Streptococcus pneumoniae infection by inhibiting the NLRP3 and TLR4/NFkappaB signaling pathway. Mol Med Rep 20(6):5345-5352 |
| abstractText | Streptococcus pneumoniaeinduced pneumonia is a common disease and major cause of communityacquired pneumonia. Previous studies have shown that Follistatinlike protein 1 (FSTL1) serves important roles in regulating the inflammatory response. The present study aimed to investigate the effect of FSTL1 on the inflammatory response during S. pneumoniae infection using in vitro and in vivo models. ELISAs were used to detect the production of interleukin (IL)1beta, tumor necrosis factoralpha and IL6. Western blotting and reverse transcriptionquantitative PCR were performed to determine the protein and mRNA expression of these factors. The results of the present study indicated that S. pneumoniae infection triggered a strong proinflammatory response and a high level of FSTL1 expression in mouse bone marrowderived macrophages. Moreover, FSTL1 may be required for the production of inflammatory factors during S. pneumoniae infection by regulating nucleotide oligomerization domainlike receptor protein 3 in vitro and in vivo. In addition, it was found that the Tolllike receptor 4/nuclear factorkappaB signaling pathway was involved in the inflammatory response regulated by FSTL1. The findings of the present study suggested that FSTL1 plays an important role in the inflammatory response during S. pneumoniae infection, providing a potential therapeutic target for reducing morbidity and mortality in patients with pneumonia. |
