ArticleNature communications2021
Reprogramming of microRNA expression via E2F1 downregulation promotes Salmonella infection both in infected and bystander cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Host miRNA orchestration of mitophagy pathways during bacterial infection: current advances and future directions.Frontiers in microbiology · 2026Review
- miR-215 Modulates Ubiquitination to Impair Inflammasome Activation and Autophagy DuringAnimals : an open access journal from MDPI · 2025Article
- Non-coding RNA Networks in Infection.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Role of microRNAs in immunoregulatory functions of epithelial cells.BMC immunology · 2024Review
- 5'isomiR-183-5p|+2 elicits tumor suppressor activity in a negative feedback loop with E2F1.Journal of experimental & clinical cancer research : CR · 2022Article
- Study of microRNA expression in Salmonella Typhimurium-infected porcine ileum reveals miR-194a-5p as an important regulator of the TLR4-mediated inflammatory response.Veterinary research · 2022Article
- Understanding microRNAs in the Context of Infection to Find New Treatments against Human Bacterial Pathogens.Antibiotics (Basel, Switzerland) · 2022Review
- Computational prediction and experimental validation ofFrontiers in cellular and infection microbiology · 2022Article
- E2F transcription factor 1 elevates cyclin D1 expression by suppressing transcription of microRNA-107 to augment progression of glioma.Brain and behavior · 2021Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells infected with pathogens can contribute to clearing infections by releasing signals that instruct neighbouring cells to mount a pro-inflammatory cytokine response, or by other mechanisms that reduce bystander cells' susceptibility to infection. Here, we show the opposite effect: epithelial cells infected with Salmonella Typhimurium secrete host factors that facilitate the infection of bystander cells. We find that the endoplasmic reticulum stress response is activated in both infected and bystander cells, and this leads to activation of JNK pathway, downregulation of transcription factor E2F1, and consequent reprogramming of microRNA expression in a time-dependent manner. These changes are not elicited by infection with other bacterial pathogens, such as Shigella flexneri or Listeria monocytogenes. Remarkably, the protein HMGB1 present in the secretome of Salmonella-infected cells is responsible for the activation of the IRE1 branch of the endoplasmic reticulum stress response in non-infected, neighbouring cells. Furthermore, E2F1 downregulation and the associated microRNA alterations promote Salmonella replication within infected cells and prime bystander cells for more efficient infection.
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