Dataset Information

Coxiella burnetii infects JEG trophoblastic cell line, a model of placenta infection

ABSTRACT: Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium usually found in myeloid cells. The infection is a source of severe obstetrical complications in humans and cattle, and of chronic evolution in pregnant women. As C. burnetii is found in the placenta of aborted foetuses in humans and ruminants, we wondered if it may infect trophoblasts. In this work, we showed that C. burnetii, infected JEG trophoblastic cells without replication and was localized within phagolysosomes. We analyzed gene expression programs induced by C. burnetii in JEG trophoblastic cell line and compared it with transcriptomic program of BeWo trophoblasts in which C. burnetii replicates. These transcriptomic programs induced by C. burnetii in JEG trophoblasts was poor and markedly different from that induced by C. burnetii in BeWo trophoblasts. Hence, the differences in transcriptomic programs may explain the different intracellular fate of C. burnetii in JEG and BeWo cells. Our results suggest that C. burnetii may use trophoblastic cells as a reservoir by interfering with gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30330 | GEO | 2012/12/07

SECONDARY ACCESSION(S): PRJNA143619

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Pre-existing and gestationally-developed diabetes mellitus during pregnancy have been linked to impaired metabolic function in the villous trophoblast layer of the placenta. These metabolic impairments have been thought to mediate an increased risk of early life metabolic disease development in the exposed offspring. Previous research using the BeWo trophoblast cell line has suggested that independently, hyperglycemia is an important modulator of placental metabolic function in diabetic pregnancies. However, the direct impacts of hyperglycemia on specific aspects of placental metabolic function known to be impaired in diabetic pregnancies including nutrient storage and mitochondrial respiration, are largely unknown. The current study, therefore, utilized functional readouts of metabolic enzyme activity and endpoint readouts of nutrient storage in conjunction with multi-omics analysis (transcriptomics and metabolomics) in BeWo trophoblasts cultured under hyperglycemia conditions (25 mM glucose) for 72 hours to further characterize the impacts of elevated glucose levels on placental metabolic function. While metabolic enzyme activities and mitochondrial oxidative respiratory function were not altered following 72 hours of hyperglycemia, increased triglyceride and glycogen nutrient stores were observed in the high-glucose exposed BeWo trophoblasts. We speculated that the increased nutrient stores serve to modulate intracellular glucose levels and may reduce the amount of glucose available for oxidation and subsequently protect trophoblast cells from mitochondrial damage during acute high glucose exposures. Additionally, hyperglycemic-culture conditions in BeWo trophoblasts were associated with an altered transcriptomic profile highlighted by altered mRNA expression of metabolic enzymes as well as with an altered metabolome profile highlighted by an intracellular accumulation of lactate, malonate, and riboflavin. Overall, the results demonstrate that exposure to excess glucose modulates placental metabolism and nutrient storage and highlights that increased glucose abundance is an important independent regulator of placental function in diabetic pregnancies.

Dataset Information

Coxiella burnetii infects JEG trophoblastic cell line, a model of placenta infection

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets