TRIM27 suppresses inflammation injuries in pediatric pneumonia by targeting TLR4/NF-κB signaling pathway.

Abstract

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.