Dataset Information

Quantification of host proteomic responses to hepatitis E virus replication facilitated by pregnancy serum

ABSTRACT: In this study, the differences in the proteomics of HEV-infected HepG2 cells supplemented with fetal bovine serum (FBS) from those of HEV-infected HepG2 cells supplemented with serum from women in their third trimester of pregnancy were quantified by using isobaric tags for relative and absolute quantification (iTRAQ) technology.

ORGANISM(S): Hepatitis E Virus

SUBMITTER: Fen Huang

PROVIDER: PXD036836 | iProX | Fri Sep 16 00:00:00 GMT+01:00 2022

REPOSITORIES: iProX

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Publications

Quantification of host proteomic responses to genotype 4 hepatitis E virus replication facilitated by pregnancy serum.

Qian Zhongyao Z Cong Chao C Li Yi Y Bi Yanhong Y He Qiuxia Q Li Tengyuan T Xia Yueping Y Xu Liangheng L Mickael Houfack K HK Yu Wenhai W Liu Jiankun J Wei Daqiao D Huang Fen F

Virology journal 20230601 1

<h4>Background</h4>Hepatitis E virus (HEV) infection is a common cause of acute hepatitis worldwide and causes approximately 30% case fatality rate among pregnant women. Pregnancy serum (PS), which contains a high concentration of estradiol, facilitates HEV replication in vitro through the suppression of the PI3K-AKT-mTOR and cAMPK-PKA-CREB signaling pathways. However, the proteomics of the complex host responses to HEV infection, especially how PS facilitates viral replication, remains unclear. ...[more]

PMID: 37264422

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Project description:The bacterial pathogen Listeria monocytogenes breaches the placental barrier and infects the placental/fetal unit resulting in poor pregnancy outcomes. L. monocytogenes is thought to enter the placenta by infection of trophoblasts at the maternal/fetal interface. Trophoblasts are fetal epithelial cells that delineate the maternal/fetal interface and ensure critical functions by promoting all nutritional and waste exchanges between maternal and fetal bloods and by forming a protective immune barrier. In this work, we report the first transcriptomic analysis of L. monocytogenes-infected trophoblasts by RNA sequencing. Primary human trophoblasts (PHT) and BeWo (fused and non-fused) were infected for 5 h with WT L. monocytogenes and highly purified RNA was extracted from infected and control cells. A 200 ng total RNA sample was used for sequencing on Illumina NovaSeq SP flowcell in paired-end 150 bp format to a read yield between 70-80 million reads. Pathway analysis showed that infection upregulated TLR2-, NOD-like, and cytosolic DNA sensing pathways, as well as downstream pro-inflammatory circuitry (NF-KB, AP-1, IRF4, IRF7) leading to the production of mediators known to elicit the recruitment and activation of maternal leukocytes (IL8, IL6, TNFA, MIP-1). Signature genes associated with poor pregnancy outcomes were also upregulated upon infection. Measuring the release of 54 inflammatory mediators confirmed the transcriptomic data and revealed sustained production of tolerogenic factors (IL-27, IL-10, IL-1RA, TSLP) despite infection. Both the SYN and mononuclear trophoblasts produced cytokines, but surprisingly, some cytokines were predominantly produced by the SYN (IL-8, IL-6) or by non-fused trophoblasts (TNFA). Collectively, our data support that trophoblasts act as placental gatekeepers that limit and detect L. monocytogenes infection resulting in a pro-inflammatory response, which may contribute to the poor pregnancy outcomes if the pathogen persists.

Dataset Information

Quantification of host proteomic responses to hepatitis E virus replication facilitated by pregnancy serum

Publications

Quantification of host proteomic responses to genotype 4 hepatitis E virus replication facilitated by pregnancy serum.

Similar Datasets

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