Potential Late Effects of Early Pregnancy Night-Shift Exposure on Hofbauer Cells in Term Placentas: A Histological and Ultrastructural Study

Abstract

Background Night shift work is considered an important environmental stressor with the potential to disrupt circadian rhythm and adversely affect placental structure and function during pregnancy. Materials and methods In this study, microscopic placental changes in pregnant women working regular daytime schedules (Group 1, n = 45) were compared with those of pregnant women who worked night shifts before pregnancy and during the first 24 weeks of gestation (Group 2, n = 45). Term placental samples were evaluated using hematoxylin and eosin (H&E) staining, along with immunostaining for phospho-BMAL1, CLOCK, and melatonin 1 A. Additionally, double immunofluorescence staining for CD68/CD163 and transmission electron microscopy analyses were performed. Results While the overall villous architecture remained largely preserved in both groups, the night-shift work group exhibited a higher frequency of microscopic lesions, including villous edema, abnormal vascularization, and hemorrhage. The mean histopathological damage score (MHDS) was significantly higher in group 2 (4.93 +/- 1.92) than in group 1 (2.29 +/- 1.10) (p < 0.001). Immunohistochemical analysis revealed significantly decreased expression of phospho-BMAL1, CLOCK, and melatonin receptor 1 A (MTNR1A) in group 2 (all p < 0.001). Immunofluorescence analysis revealed an increased number of CD68(+), CD163(+), and CD68(+)CD163(+) double-positive cells in group 2 (p < 0.005). Ultrastructural evaluation showed irregular microvilli and thickening/irregularity of the trophoblastic basal lamina in night-shift placentas. Conclusion In conclusion, night-shift work is associated with increased histopathological damage in the placenta, reduced circadian marker expression, and altered placental immune cell dynamics. Overall, these results indicate that circadian disruption related to night-shift work affects placental structure, molecular clock regulation, and immune microenvironment.