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Background <p>Severe pneumonia in children typically presents with the most prominent early lesion being damage to the bronchial mucosa.</p> Aim <p>To explore the diagnostic value of hsa_circ_0077658 in pediatric severe pneumonia and its possible mechanism of action.</p> Materials and methods <p>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.</p> Results <p>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, overexpression of NF1 can reverse the exacerbating effect of miR-15a-5p overexpression on the damage caused by LPS to BEAS-2B cells.</p> Conclusion <p>Hsa_circ_0077658 may be a biomarker for pediatric severe pneumonia, potentially influencing disease progression via the miR-15a-5p/NF1 axis.</p>

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Hsa_circ_0077658 serves as a potential diagnostic biomarker for severe pneumonia in children and alleviates lipopolysaccharide-induced damage to bronchial epithelial cells by modulating the miR-15a-5p/NF1 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月24日

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  • Hui Zhang,
  • Chang Liu,
  • Hui Qi,
  • Mei Yang

摘要

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, overexpression of NF1 can reverse the exacerbating effect of miR-15a-5p overexpression on the damage caused by LPS to BEAS-2B cells.

Conclusion

Hsa_circ_0077658 may be a biomarker for pediatric severe pneumonia, potentially influencing disease progression via the miR-15a-5p/NF1 axis.