ITGAM and FCGR3B contribute to recurrent and limited CRSwNP in children through phagosome pathway.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is more common in children with limited CRSwNP (L-CRSwNP). L-CRSwNP shares similar clinical phenotypes with recurrent CRSwNP (R-CRSwNP). This study aimed to explore the molecular mechanisms of L- and R-CRSwNP in children. Compared clinical characteristics and RNA sequencing data of 20 L-CRSwNP and 5 R-CRSwNP in children. Paired analyzed RNA sequencing data of 6 children with L-CRSwNP polyps and mucosal tissue samples. Conducted GO and KEGG enrichment analyses. Identified hub genes through protein-protein interaction networks (PPI). Validated hub genes in L- and R-CRSwNP using real-time quantitative PCR (RT-qPCR), immunohistochemistry (IHC), and multiplex immunohistochemistry (mIHC). RNA-seq analysis of L- and R-CRSwNP polyp showed no differentially expressed genes (DEGs). RNA-seq paired analysis of L-CRSwNP identified 1419 DEGs. GO enrichment analysis showed significant enrichment for biological processes associated with neutrophils. ITGAM and FCGR3B were identified as hub genes by PPI analysis. RT-qPCR and IHC results suggested the expression levels of ITGAM and FCGR3B were significantly increased in L- and R-CRSwNP. mIHC results suggested ITGAM and FCGR3B were closely associated with neutrophils and M2 macrophages in L- and R-CRSwNP. L- and R-CRSwNP in children exhibit similar clinical phenotypes and molecular mechanisms. ITGAM and FCGR3B are hub genes contributing to disease through neutrophil- and M2 macrophage-mediated phagosome pathway.