Downregulation of FSTL‑1 attenuates the inflammation injury during Streptococcus pneumoniae infection by inhibiting the NLRP3 and TLR4/NF‑κB signaling pathway

Chen,Liang; Liu,Zhenshe

doi:10.3892/mmr.2019.10752

Downregulation of FSTL‑1 attenuates the inflammation injury during Streptococcus pneumoniae infection by inhibiting the NLRP3 and TLR4/NF‑κB signaling pathway

Authors:
- Liang Chen
- Zhenshe Liu
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Affiliations: Department of Infectious Disease, Beijing Jishuitan Hospital, 4th Medical College of Peking University, Beijing 100096, P.R. China, Department of Laboratory, Xian Yang Central Hospital, Xianyang, Shaanxi 712000, P.R. China
Published online on: October 16, 2019 https://doi.org/10.3892/mmr.2019.10752
Pages: 5345-5352

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Abstract

Streptococcus pneumoniae‑induced pneumonia is a common disease and major cause of community‑acquired pneumonia. Previous studies have shown that Follistatin‑like protein 1 (FSTL‑1) serves important roles in regulating the inflammatory response. The present study aimed to investigate the effect of FSTL‑1 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)‑1β, tumor necrosis factor‑α and IL‑6. Western blotting and reverse transcription‑quantitative 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 FSTL‑1 expression in mouse bone marrow‑derived macrophages. Moreover, FSTL‑1 may be required for the production of inflammatory factors during S. pneumoniae infection by regulating nucleotide oligomerization domain‑like receptor protein 3 in vitro and in vivo. In addition, it was found that the Toll‑like receptor 4/nuclear factor‑κB signaling pathway was involved in the inflammatory response regulated by FSTL‑1. The findings of the present study suggested that FSTL‑1 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.

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