Epigenetic signature of exposure to maternal Trypanosoma cruzi infection in cord blood cells from uninfected newborns

Epigenomics. 2022 Aug;14(15):913-927. doi: 10.2217/epi-2022-0153. Epub 2022 Aug 29.

Abstract

Aims: To assess the epigenetic effects of in utero exposure to maternal Trypanosoma cruzi infection. Methods: We performed an epigenome-wide association study to compare the DNA methylation patterns of umbilical cord blood cells from uninfected babies from chagasic and uninfected mothers. DNA methylation was measured using Infinium EPIC arrays. Results: We identified a differential DNA methylation signature of fetal exposure to maternal T. cruzi infection, in the absence of parasite transmission, with 12 differentially methylated sites in B cells and CD4+ T cells, including eight protein-coding genes. Conclusion: These genes participate in hematopoietic cell differentiation and the immune response and may be involved in immune disorders. They also have been associated with several developmental disorders and syndromes.

Keywords: Chagas disease; DNA methylation; Trypanosoma cruzi; parasite; pregnancy.

Plain language summary

Maternal infection with Trypanosoma cruzi, the parasite that causes Chagas disease, may influence fetal development, even in the absence of parasite transmission. Thus we investigated how exposure to maternal infection might lead to changes in gene expression in the infant, by examining changes in DNA methylation in the umbilical cord blood. We found that exposure to maternal infection alters DNA methylation of at least 12 sites, including eight genes. Expression of these genes may be altered, which may affect blood cell function, the immune response and newborn development later in life. Further studies should monitor newborns from infected mothers to better assess their health and possible longer term effects.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Chagas Disease* / genetics
  • Chagas Disease* / metabolism
  • DNA Methylation
  • Epigenesis, Genetic
  • Epigenomics
  • Female
  • Fetal Blood* / metabolism
  • Humans
  • Infant
  • Infant, Newborn
  • Maternal Exposure
  • T-Lymphocytes