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Small RNA sequencing reveals placental miRNAs linked to congenital transmission of Trypanosoma cruzi

ABSTRACT: Background: Congenital transmission remains an important source of new Chagas disease cases. This study aimed to identify placental microRNAs (miRNAs) associated with congenital transmission of Trypanosoma cruzi. Methods: Placental samples from T. cruzi-infected mothers were classified according to congenital transmission status and analyzed by small RNA sequencing. Differential expression was assessed using DESeq2 with Benjamini-Hochberg false discovery rate correction. Nine candidate miRNAs were subsequently assessed by RT-qPCR. Results: Small RNA sequencing was performed in 31 placental samples, including 13 from transmitting mothers and 18 from non-transmitting mothers. hsa-miR-155-5p was the only miRNA significantly upregulated in placentas from transmitting mothers after multiple-testing correction and was selected as a candidate for further validation. Seven additional miRNAs (hsa-miR-193a-5p, hsa-miR-187-3p, hsa-miR-512-5p, hsa-miR-515-5p, hsa-miR-526a-5p, hsa-miR-99b-3p, and hsa-miR-455-5p) were selected based on nominal p-value, expression abundance, and differences in mean normalized counts between groups. RT-qPCR assessment in 15 placental samples, including 5 from transmitting mothers and 10 from non-transmitting mothers, showed higher normalized expression of hsa-miR-193a-5p and hsa-miR-187-3p in transmitting mothers.Conclusion: Placental miRNA profiling identified hsa-miR-155-5p, hsa-miR-193a-5p, and hsa-miR-187-3p as candidates for further investigation in congenital transmission of T. cruzi. These findings require confirmation in larger cohorts.

ORGANISM(S): Homo sapiens

PROVIDER: GSE333874 | GEO | 2026/06/04

REPOSITORIES: GEO

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Project description:Background. More than one million women in fertile age are infected with Trypanosoma cruzi worldwide. Anti-T.cruzi seropositivity in mothers has been associated with adverse pregnancy outcome but there is still a knowledge gap regarding this effect. Our aim was to compare the gene expression profile of term placental environment from T. cruzi seropositive (SP) and seronegative (SN) mothers. Methods. A RNA-Seq was performed in 9 pools of 2 different placental RNA samples each: 3 belonging to placentas from SN and 6 from SP. Each pool consisted of a binomial of a female/male newborn and a vaginal/caesarean delivery. None of the newborns resulted infected. Results. Only 42 genes showed a significant fold change between SP and SN groups. Among the down-regulated genes were KISS1 and CGB5. In the up-regulated genes group were: KIF12, HLA-G, PRG2, TAC3, FN1 and ATXN3L. To identify pathways significantly associated with maternal T. cruzi-infection, a gene-set association analysis was implemented. The placental environment transcriptomic profile of SP consisted of an enrichment in immunological genes sets (inflammatory response and lymphocytic activation were over-expressed) whereas numerous biosynthetic processes were down-regulated. Conclusions. It is worth noting that several differentially expressed genes in SP placentas code for proteins associated to preeclampsia and miscarriage. This first transcriptomics study in human term placental environment from non-infected deliveries shows a placental response that may affect the faetus while protecting it from the parasite infection; this host response could be responsible for the low rate of congenital transmission observed in human chronic Chagas disease. Background. More than one million women in fertile age are infected with Trypanosoma cruzi worldwide. Anti-T.cruzi seropositivity in mothers has been associated with adverse pregnancy outcome but there is still a knowledge gap regarding this effect. Our aim was to compare the gene expression profile of term placental environment from T. cruzi seropositive (SP) and seronegative (SN) mothers. Methods. A RNA-Seq was performed in 9 pools of 2 different placental RNA samples each: 3 belonging to placentas from SN and 6 from SP. Each pool consisted of a binomial of a female/male newborn and a vaginal/caesarean delivery. None of the newborns resulted infected. Results. Only 42 genes showed a significant fold change between SP and SN groups. Among the down-regulated genes were KISS1 and CGB5. In the up-regulated genes group were: KIF12, HLA-G, PRG2, TAC3, FN1 and ATXN3L. To identify pathways significantly associated with maternal T. cruzi-infection, a gene-set association analysis was implemented. The placental environment transcriptomic profile of SP consisted of an enrichment in immunological genes sets (inflammatory response and lymphocytic activation were over-expressed) whereas numerous biosynthetic processes were down-regulated. Conclusions. It is worth noting that several differentially expressed genes in SP placentas code for proteins associated to preeclampsia and miscarriage. This first transcriptomics study in human term placental environment from non-infected deliveries shows a placental response that may affect the faetus while protecting it from the parasite infection; this host response could be responsible for the low rate of congenital transmission observed in human chronic Chagas disease.

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Small RNA sequencing reveals placental miRNAs linked to congenital transmission of Trypanosoma cruzi

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