Abstract

Background: Severe pneumonia in children typically presents with the most prominent early lesion being damage to the bronchial mucosa. Aim: To explore the diagnostic value of hsa_circ_0077658 in pediatric severe pneumonia and its possible mechanism of action. Materials and methods: 116 children with severe pneumonia, 87 children with pneumonia, and 60 healthy children were included. Lipopolysaccharide (LPS) was used to stimulate BEAS-2B cells to establish a pneumonia cell model. Reverse Transcription quantitative PCR (RT-qPCR) was performed to detect the expression levels of hsa_circ_0077658, miR-15a-5p and Neurofibromatosis type 1(NF1). The Enzyme-Linked Immunosorbent Assay (ELISA) method was performed to detect the levels of oxidative stress markers and inflammatory factors. The Annexin V/PI and Cell Counting Kit-8 (CCK-8) kits were used to assess the apoptosis and proliferation levels of BEAS-2B cells, respectively. Person's correlation analysis, dual luciferase assays and RNA Binding Protein Immunoprecipitation (RIP) experiments were performed to demonstrate the relationship between genes. Results: Hsa_circ_0077658 and NF1 were downregulated in patients with pneumonia and in LPS-induced BEAS-2B cells, while miR-15a-5p was upregulated. Hsa_circ_0077658 showed excellent diagnostic performance, with an AUC of 0.820 (95% CI: 0.749-0.890) in healthy vs. pneumonia children comparison and 0.931 (95% CI: 0.894-0.966) for distinguishing pneumonia children from severe pneumonia children. Following exposure to LPS, BEAS-2B cells exhibited heightened oxidative stress, apoptosis, and inflammatory responses, while cellular proliferation was suppressed. Hsa_circ_0077658 targets miR-15a-5p, and NF1 is the downstream effect target of miR-15a-5p. Overexpression of hsa_circ_0077658 can alleviate the oxidative stress, apoptosis and inflammatory response in LPS-BEAS-2B cells, thereby promoting proliferation. This effect was reversed by overexpression of miR-15a-5p. Furthermore, ove