Abstract:

Lower reproductive tract infection in women is a common gynecological disorder with a complex pathogenesis. The core pathological processes include vaginal mucosal epithelial cell injury and disruption of barrier function. The vaginal mucosal epithelium serves not only as a physical barrier but also participates in local immune regulation, with its function being influenced by multiple factors such as inflammation, microbiota, and hormonal levels. Cold-inducible RNA-binding protein (CIRP), as a novel damage-associated molecular pattern (DAMP), plays a pivotal role in inflammation and barrier damage in various mucosal tissues. Studies have shown that CIRP can interact with Toll-like receptor 4 (TLR4) and triggering receptor expressed on myeloid cells-1 (TREM-1), activating the nuclear factor-κB signaling pathway, inducing oxidative stress, neutrophil extracellular traps (NETs) formation, and inflammation, ultimately leading to vaginal mucosal epithelial cell apoptosis and structural damage. Although the role of CIRP in mucosal injury in tissues such as the intestine and respiratory tract is well-established, its specific mechanism in vaginal mucosal epithelial injury remains to be elucidated. Based on existing literature, it is hypothesized that CIRP may mediate vaginal mucosal epithelial damage by regulating inflammatory signal transduction, inducing epithelial cell apoptosis, and disrupting intercellular junctions, thereby promoting the occurrence and recurrence of lower reproductive tract infection. Future research should focus on constructing in vitro organ-on-a-chip models to examine the interactions among CIRP, the hormonal cycle, local immunity, and vaginal microbiota, and explore intervention strategies based on CIRP regulation, with the aim of providing new insights for the prevention and treatment of female lower reproductive tract infection.

Key words: Cold-inducible RNA-binding protein, RNA-binding proteins, Organ-on-a-chip model, Vaginal mucosal barrier, Lower reproductive tract infection, Neutrophil extracellular traps