Department of Pediatric Ward Six, Lu'an People's Hospital, Luan Hospital Affiliated of Anhui Medical University, Lu'an, Anhui Province, China.
Department of Pediatric, The People's Hospital of Yubei District of Chongqing City, Chongqing, China;
Allergol Immunopathol (Madr). 2022 Mar 1;50(2):33-39. doi: 10.15586/aei.v50i2.558. eCollection 2022.
Pneumonia widely occurs in children and has high global morbidity and mortality. There is an urgent requirement to clarify the underlying mechanism of pediatric pneumonia and definite its potential therapeutic targets. Tri-domain protein 27 (TRIM27) is one of the TRIM protein family members which widely participated in multiple cellular processes.
To assess whether TRIM27 protects against pediatric pneumonia.
A lipopolysaccharide (LPS)-induced inflammation injury model was constructed. The level of TRIM27 in LPS-induced cells was examined. The effects of TRIM27 in cell apoptosis and inflammatory response was evaluated. Moreover, the involvement of TLR4/NF-κB pathway were detected by Immunoblot.
We established a lipopolysaccharide (LPS)-induced inflammation injury model. Our data confirmed that LPS-treated WI-38 cells demonstrated a down-regulated expression of TRIM27. Overexpression of TRIM27 effectively reduced apoptosis and up-regulated the inflammatory factors in LPS-treated WI-38 cells. Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) pathway acted as a key point in LPS-mediated inflammation injuries, and overexpression of TRIM27 remarkably inhibited the activity of TLR4/NF-κB pathway, indicating the anti-inflammatory effect of TRIM27.
In conclusion, TRIM27 protects WI-38 cells against LPS-induced inflammation injuries by inhibiting TLR4/NF-κB pathway.
肺炎在儿童中广泛发生，具有较高的全球发病率和死亡率。迫切需要阐明小儿肺炎的发病机制，明确其潜在的治疗靶点。三结构域蛋白 27（TRIM27）是 TRIM 蛋白家族成员之一，广泛参与多种细胞过程。
评估 TRIM27 是否对小儿肺炎起保护作用。
构建脂多糖（LPS）诱导的炎症损伤模型。检测 LPS 诱导细胞中 TRIM27 的水平。评估 TRIM27 对细胞凋亡和炎症反应的影响。此外，通过免疫印迹检测 TLR4/NF-κB 通路的参与情况。
我们建立了脂多糖（LPS）诱导的炎症损伤模型。我们的数据证实，LPS 处理的 WI-38 细胞中 TRIM27 的表达下调。TRIM27 的过表达可有效减少细胞凋亡并上调 LPS 处理的 WI-38 细胞中的炎症因子。Toll 样受体 4（TLR4）/核因子 kappa B（NF-κB）通路是 LPS 介导的炎症损伤的关键环节，TRIM27 的过表达显著抑制 TLR4/NF-κB 通路的活性，表明 TRIM27 具有抗炎作用。
综上所述，TRIM27 通过抑制 TLR4/NF-κB 通路来保护 WI-38 细胞免受 LPS 诱导的炎症损伤。
