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.
Conclusion
This study identified some candidate differential proteins, such as NQO1, CD36, S100A2, and the inflammation pathways involved in adenoid hypertrophy in preschool children.
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.