Decreased IL-33 Expression in the Cervix in LPS-Induced Preterm Birth and the Potential Role of Mast Cells: A Murine Model

Abstract

Problem: In order to gain a deeper understanding of the mechanisms underlying LPS-mediated preterm birth, it is crucial to investigate the relationship between preterm birth and mast cells (MCs). Moreover, the role of antihistamines in inflammatory processes during pregnancy remains incompletely understood. Method of Study: CD-1 female mice were administered intrauterine lipopolysaccharide (LPS) via midline laparotomy to establish an inflammation-induced preterm birth model. The experimental groups (n = 6 per group) were formed as Nonpregnant and pregnant control, Sham, PBS, LPS, Cetirizine (CET) control, and two CET treatment groups (CET 10 mg/kg-low dose, and CET 20 mg/kg-high dose with LPS administration). Tissue samples were analyzed using immunohistochemistry and Western blot techniques. Results: Our findings suggest that MCs play a significant role in preterm birth, with LPS administration inducing MC dysfunction in the reproductive tract during pregnancy. Additionally, high doses of CET may support inflammatory responses. A particularly notable result was the reduction in interleukin-33 (IL-33) expression in the cervix during LPS-induced preterm birth. This suggests that IL-33 may serve as a potential biomarker for preterm birth in the cervix. Conclusions: The effects of CET during LPS-mediated preterm birth appear to be dose-dependent, warranting further exploration of their role in this context.