ArticlePloS one2013
Route of Infection Determines the Impact of Type I Interferons on Innate Immunity to Listeria monocytogenes.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- The dual role of type I interferons in bacterial infections: from immune defense to pathogenesis.mBio · 2025Review
- For Better or Worse: Type I Interferon Responses in Bacterial Infection.Pathogens (Basel, Switzerland) · 2025Review
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Genetic and immune determinants ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Genetic and immune determinants ofbioRxiv : the preprint server for biology · 2023Article
- Review
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
- Listeria monocytogenes infection rewires host metabolism with regulatory input from type I interferons.PLoS pathogens · 2021Article
- Type I interferon remodels lysosome function and modifies intestinal epithelial defense.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Secretion of c-di-AMP by Listeria monocytogenes Leads to a STING-Dependent Antibacterial Response during Enterocolitis.Infection and immunity · 2020Article
- Thyroid stimulating hormone β-subunit splice variant is expressed in all fractional subsets of bone marrow hematopoietic cells and peripheral blood leukocytes and is modulated during bacterial infection.General and comparative endocrinology · 2020Article
- Type I Interferons Ameliorate Zinc Intoxication of Candida glabrata by Macrophages and Promote Fungal Immune Evasion.iScience · 2020Article
- Pathogenic Biohacking: Induction, Modulation and Subversion of Host Transcriptional Responses byToxins · 2020Review
- The Systemic and Cellular Metabolic Phenotype of Infection and Immune Response toFrontiers in immunology · 2020Article
- Context Is Key: Delineating the Unique Functions of IFNα and IFNβ in Disease.Frontiers in immunology · 2020Review
- Validation of Predicted Virulence Factors inToxins · 2019Article
- Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019Article
- Sources of Type I Interferons in Infectious Immunity: Plasmacytoid Dendritic Cells Not Always in the Driver's Seat.Frontiers in immunology · 2019Review
- A Comparison of Oral and Intravenous Mouse Models of Listeriosis.Pathogens (Basel, Switzerland) · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Listeria monocytogenes is a food-borne pathogen which causes mild to life threatening disease in humans. Ingestion of contaminated food delivers the pathogen to the gastrointestinal tract, where it crosses the epithelial barrier and spreads to internal organs. Type I interferons (IFN-I) are produced during infection and decrease host resistance after systemic delivery of L. monocytogenes. Here we show that mice benefit from IFN-I production following infection with L. monocytogenes via the gastrointestinal route. Intragastric infection lead to increased lethality of IFN-I receptor chain 1-deficient (Ifnar1-/-) animals and to higher bacterial numbers in liver and spleen. Compared to infection from the peritoneum, bacteria infecting via the intestinal tract localized more often to periportal and pericentral regions of the liver and less frequently to the margins of liver lobes. Vigorous replication of intestine-borne L. monocytogenes in the livers of Ifnar1-/- mice 48 h post infection was accompanied by the formation of large inflammatory infiltrates in this organ and massive death of surrounding hepatocytes. This was not observed in Ifnar1-/- mice after intraperitoneal infection. The inflammatory response to infection is shaped by alterations in splenic cytokine production, particularly IFNγ, which differs after intragastric versus intraperitoneal infection. Taken together, our data suggest that the adverse or beneficial role of a cytokine may vary with the route of infection and that IFN-I are not harmful when infection with L. monocytogenes occurs via the natural route.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.