IL-37 and 38 signalling in gestational diabetes

Area of Science:

• Reproductive immunology
• Maternal-fetal medicine
• Inflammatory diseases

Background:

• Gestational diabetes mellitus (GDM) poses a global health challenge, with inflammation implicated in its pathogenesis.
• The specific roles of Interleukin-37 (IL-37) and Interleukin-38 (IL-38) in GDM development remain largely unexplored.
• Existing research highlights the involvement of IL-37 and IL-38 in autoimmune conditions, prompting investigation into their function in pregnancy.

Purpose of the Study:

• To investigate the expression levels of IL-37 and IL-38 in placental and umbilical cord tissues of women with GDM compared to non-GDM controls.
• To determine the correlation between IL-37 and IL-38 levels and the development of GDM.
• To elucidate the potential immune-mediated mechanisms underlying GDM pathogenesis involving these cytokines.

Main Methods:

• Histopathology and immunohistochemistry were employed to assess placental and umbilical cord tissue characteristics.
• Quantitative real-time PCR (qRT-PCR) was used to measure placental mRNA expression of IL-37 and IL-38.
• Enzyme-linked immunosorbent assay (ELISA) was utilized to evaluate serum levels of IL-37 and IL-38.

Main Results:

• IL-37 expression was significantly reduced in the chorionic villi, umbilical artery, and umbilical vein of GDM placentas compared to controls.
• Conversely, IL-38 expression was markedly increased in the chorionic villi, umbilical artery, and umbilical vein of GDM placentas.
• Reduced IL-37 and elevated IL-38 levels were also observed in the serum of women with GDM.

Conclusions:

• The findings suggest that decreased IL-37 may protect pregnant women against GDM development.
• Elevated IL-38 in placental and umbilical cord tissues may represent a localized inflammatory response during GDM progression.
• The observed dysregulation of IL-37 and IL-38 points towards an immune-mediated mechanism contributing to GDM pathogenesis, offering potential targets for intervention.