Table 1_Sequential exposure to histological chorioamnionitis and postnatal hyperoxia alters gene expression in cord blood monocytes.docx

Compared with no HCA–Normoxia, HCA alone exhibited 1,195 differentially expressed genes, with transcriptional signatures consistent with monocyte activation and differentiation (including CLEC5A, FCGR3A, FCGR2B, CD101, PRAM1, and FN1 upregulation). Hyperoxia alone yielded 533 differentially expressed genes, while sequential exposure to HCA–Hyperoxia led to 1,599 differentially expressed genes. Hyperoxia without HCA demonstrated upregulated genes associated with inflammatory signaling and immune modulation (including CXCL8, TM4SF19, and PLPP3) and downregulated genes involved in pathogen recognition and monocyte survival (TLR6, TLR8, and PECAM1).

Sequential HCA–Hyperoxia exposure was associated with a broader transcriptional response, with upregulation of pro-inflammatory and pro-fibrotic genes (CLEC5A, FN1, and CCL24) and downregulation of immune regulatory genes (USP18, TMEM176B, and HLA-DQB1). Pathway analysis revealed alterations in immune and inflammatory signaling, antigen presentation, neutrophil degranulation, protein ubiquitination, and metabolic regulation.</p>Conclusions<p>Sequential exposure to histological chorioamnionitis and postnatal hyperoxia induces alterations in gene expression and molecular pathways in neonatal cord blood monocytes, affecting immune regulation, which could potentially contribute to the pathogenesis of short- and long-term diseases.</p>