Diagnostic and Prognostic Value of miR-27a-5p in Childhood Severe Pneumonia Through Targeted Regulation of FOXO1.
In children with pneumonia, the study reports higher miR-27a-5p in severe disease, diagnostic and prognostic associations, and cell-based evidence that miR-27a-5p targets FOXO1 and affects viability, apoptosis, and inflammatory-factor production.
Open original publication →What the AI sees
In children with pneumonia, the study reports higher miR-27a-5p in severe disease, diagnostic and prognostic associations, and cell-based evidence that miR-27a-5p targets FOXO1 and affects viability, apoptosis, and inflammatory-factor production.
Research significance
The evidence supports an association between elevated miR-27a-5p and severe pediatric pneumonia plus a miR-27a-5p–FOXO1 interaction in HFL1 cells; it can be inferred, but is not clinically demonstrated, that inhibiting miR-27a-5p or restoring FOXO1 might reduce inflammatory injury.
Source abstract
Severe pneumonia in children deteriorates rapidly and is very destructive. miR-27a-5p has been shown to function in multiple cancers and inflammatory conditions, but its role in severe pneumonia is unknown. To investigate the diagnostic and prognostic value of miR-27a-5p for severe pneumonia in children. This study included 146 children with severe pneumonia as subjects and 123 children with mild pneumonia as controls. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was employed to assay miR-27a-5p and FOXO1 levels. ROC and Kaplan-Meier curves were employed to assess the diagnostic and prognostic values. Cell viability and apoptosis were determined by cell counting kit-8 (CCK-8) and flow cytometry. The concentrations of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β were measured using enzyme-linked immunosorbent assay. Luciferase reporter assay for miR-27a-5p targeting FOXO1. miR-27a-5p level was higher in severe pneumonia. miR-27a-5p has a good diagnostic and prognostic value for severe pneumonia. miR-27a-5p down-regulation promotes cell viability and inhibits apoptosis and inflammatory factor production. FOXO1 is a target of miR-27a-5p. And FOXO1 may reverse the effects of miR-27a-5p on the biological function of HFL1 cell. In conclusion, miR-27a-5p may be a potential pneumonia marker by negatively regulating FOXO1 to worsen pneumonia.