This article discusses the immune status of the mother in gestational diabetes mellitus (GDM). Normal pregnancy is characterized by a controlled state of the immune system at the early stages of pregnancy. Various immunological mediators adapt to the state of pregnancy, all of which affect maternal and fetal health. GDM, defined as impaired glucose tolerance of any degree during pregnancy, is a serious obstetric complication affecting approximately 5–10% of pregnant women worldwide. Hyperglycemia causes immune dysfunction by negatively affecting neutrophil chemotaxis, macrophage function, and phagocytic responses, making diabetic patients more susceptible to infections and associated comorbidities. The state of pregnancy along with immunological changes, imbalances of innate and adaptive cellular responses present additional health risks. Insulin plays an indispensable role in the treatment of hyperglycemia that occurs in various conditions, including in type I and type II diabetes; insulin has an anti-apoptotic effect and reduces the expression of pro-inflammatory cytokines in human endotoxemic macrophages. Metformin or sulfonylurea derivatives may also be used for the treatment of GDM. Metformin suppresses immune responses mainly through its direct effect on the cellular functions of various types of immune cells. Glyburide enhances the anti-inflammatory response and synergizes with retinoic acid. A better understanding of development if immune dysfunctions during hyperglycemia could lead to new treatments and prevention for infectious diseases and DM2 comorbidities, thereby improving infectious disease outcomes in DM2 patients. These results require further study of the role of drugs such as insulin, metformin, and glyburide in the immunoregulation of the pathophysiology of GDM.

Keywords: glyburide, gestational diabetes mellitus, pregnancy, metformin, insulin