Role of IL-17 cytokines in tubal fibrosis and infertility due to salpingitis.

This review systematically examines the etiology and pathophysiology mechanisms of infectious diseases affecting the female reproductive tract, with a specific focus on the intricate relationship between inflammatory lesions in the fallopian tubes and reproductive dysfunction. The interleukin-17 cytokine family, as pivotal inflammatory regulators, plays a central role in pathological processes of fallopian tube inflammatory responses, tissue fibrosis, and fertility impairment through a multi-faceted regulatory network. IL-17 C and IL-17 A, key members of the IL-17 family, are pivotal drivers of fibrosis. IL-17 A activates Th17 cells and T cells, promoting the release of inflammatory factors. Furthermore, IL-17 C boosts the expression of IL-17 A, establishing a positive feedback loop that amplifies both inflammatory and fibrotic responses. This exacerbates tissue damage, ultimately culminating in luminal obstruction and dysfunction that hinders gamete transport and fertilization. Although the precise pathogenic mechanisms of tubal inflammatory infertility are not fully elucidated, the detrimental impact of tubal inflammation on fertility is widely recognized. This is particularly relevant given the increasing trend of delayed childbearing. While perioperative interventions can partially mitigate infertility risk, persistent inflammatory stimulation remains the primary pathological factor driving infertility. By systematically investigating the epidemiological characteristics and pathogenesis of this condition, this study aims to enhance clinical treatment strategies.