論文 - 詳細
| RRC ID | 71097 |
|---|---|
| 著者 | Wang H, Zhang L, Li Q, Xu S, Lu R. |
| タイトル | Surface-layer protein produced by Lactobacillus crispatus JCM 2009 ameliorates lipopolysaccharide-induced inflammation through autophagy cross-talk with the NF-κB signaling pathway. |
| ジャーナル | Int J Biol Macromol |
| Abstract |
In recent years, studies on immunomodulation by surface-layer proteins (Slps) have mainly focused on Lactobacillus acidophilus, there is little information on Slp from L. crispatus and its intestinal immunomodulatory mechanisms in macrophages. In our study, the anti-inflammatory actions of Slp derived from L. crispatus JCM 2009 and its related molecular mechanisms were investigated. We initially found that incubation with Slp (5-10 μg/mL) for 4 h significantly inhibited nitric oxide (NO) and prostaglandin E2 (PGE2) production in LPS-stimulated RAW264.7 cells (P < 0.001). We then found that Slp inhibited the inflammatory response by regulating the PI3K/AKT/mTOR signaling pathway and activating autophagy in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Furthermore, ELISA and Western blotting results demonstrated that the NF-κB signaling pathway positively regulated autophagic activity to inhibit the productions of PGE2 and NO during this inflammatory response. And p65 was identified as a potentially important NF-κB signaling pathway molecule mediating the effects of Slp on the LPS-induced inflammatory response in RAW264.7 cells. Our findings provide the novel perspective that Slp exerts its anti-inflammatory effects through the activation of autophagy, making it a promising bioactive ingredient for the development of functional foods. |
| 巻・号 | 166 |
| ページ | 633-640 |
| 公開日 | 2021-1-1 |
| DOI | 10.1016/j.ijbiomac.2020.10.221 |
| PII | S0141-8130(20)34874-1 |
| PMID | 33130269 |
| MeSH | Animals Autophagy* Cell Death Cell Nucleus / metabolism Cell Survival Cytokines / biosynthesis Inflammation / metabolism* Inflammation / pathology* Inflammation Mediators / metabolism Lactobacillus crispatus / metabolism* Lipopolysaccharides Membrane Proteins / biosynthesis* Mice NF-kappa B / metabolism* Phosphatidylinositol 3-Kinases / metabolism Protein Transport Proto-Oncogene Proteins c-akt / metabolism RAW 264.7 Cells Signal Transduction* TOR Serine-Threonine Kinases / metabolism |
| リソース情報 | |
| 一般微生物 | JCM2009 |