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A Proteomic Study Based on Home Quarantine Model Identifies NQO1 and Inflammation Pathways Involved in Adenoid
Penghui Chen1,2,3, Shule Hou1,2,3, Xiuhong Pang4
1Department of Otorhinolaryngology-Head and Neck Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.
Insights
COVID-19 quarantine reduced childhood adenoid hypertrophy. Proteomics revealed decreased inflammation markers and increased NQO1, suggesting new treatment targets for this common pediatric disorder.
Area of Science:
- Pediatric Otolaryngology
- Molecular Biology
- Immunology
Background:
- Adenoid hypertrophy is a prevalent childhood condition with an unknown cause.
- The COVID-19 pandemic's home quarantine offered a unique model to study adenoid hypertrophy's pathogenesis.
- Investigating environmental impacts on adenoid hypertrophy is crucial for understanding its development.
Purpose of the Study:
- To explore the pathogenesis of pediatric adenoid hypertrophy.
- To identify potential therapeutic targets for adenoid hypertrophy.
- To analyze the proteomic changes in adenoids during the COVID-19 home quarantine period.
Main Methods:
- Label-free proteomics was employed on surgically removed adenoids before and during home quarantine.
- Bioinformatic analyses included Gene Ontology, KEGG, GSEA, and protein-protein interaction networks.
- Immunohistochemistry was used to validate protein expression changes.
Main Results:
- Home quarantine significantly altered pediatric adenoid proteomics, with 28 proteins upregulated and 92 downregulated.
- Differentially expressed proteins were enriched in pathways like leukocyte activation, inflammation, and IL-17 signaling.
- Reduced inflammation markers (TNF-α, IL-6), CD36, S100A2, and increased NQO1 were observed, potentially mitigating hypertrophy.
Conclusions:
- Long-term home quarantine impacted pediatric adenoid proteomic profiles.
- NQO1, CD36, and S100A2 emerged as candidate differential proteins.
- Inflammation-related pathways are key in preschool children's adenoid hypertrophy.
Background:
Adenoid hypertrophy is a common disorder of childhood, and has an unclear pathogenesis. At the beginning of the COVID-19 pandemic, there was a significant reduction in the incidence of adenoid hypertrophy in children under long-term home quarantine, providing a rare research model to explore the pathogenesis and treatment targets of adenoidal hypertrophy in children.
Methodology:
Before and during the home quarantine period, adenoids that underwent surgery were detected using label-free proteomics. Differences in protein expression were analyzed using Gene Ontology, the Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis, Protein-protein interaction, and immunohistochemistry analysis.
Results:
Long-term home quarantine had a profound impact on the proteomics of pediatric adenoids, with up-regulated and down-regulated proteins of 28 and 92 downregulated proteins, respectively. Functional enrichment analysis showed that the differentially expressed proteins were mainly enriched in pathways such as leukocyte activation, inflammatory response, IL-1 production, Th17 cell differentiation, and IL-17 signaling. In the home quarantine group, inflammation-related proteins (TNF-α, IL-6), CD36, and S100A2, were considerably reduced, whereas NQO1 levels increased significantly, potentially alleviating adenoid hypertrophy. NQO1, CD36, NDUFS8, and NDUFAF2 exhibited strong interactions.
Conclusion:
This study identified some candidate differential proteins, such as NQO1, CD36, S100A2, and the inflammation pathways involved in adenoid hypertrophy in preschool children.
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