ArticlePLoS pathogens2019
STAT2 dependent Type I Interferon response promotes dysbiosis and luminal expansion of the enteric pathogen Salmonella Typhimurium.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 34 citations in OpenAlex.
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- Single-cell analysis of genetically minimized Salmonella reveals effector gene cooperation in vivo.Nature microbiology · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Type 3 immune response protects againstEmerging microbes & infections · 2024Article
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- Blocking IL-17A prevents oxycodone-induced depression-like effects and elevation of IL-6 levels in the ventral tegmental area and reduces oxycodone-derived physical dependence in rats.Brain, behavior, and immunity · 2024Article
- Role of type-I and type-III interferons in gastrointestinal homeostasis and pathogenesis.Current opinion in immunology · 2024Review
- Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β.PLoS biology · 2024Article
- The crucial regulatory role of type I interferon in inflammatory diseases.Cell & bioscience · 2023Review
- Gut dysbiosis: Ecological causes and causative effects on human disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Response ofInternational journal of molecular sciences · 2022Article
- Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Bacterial Quorum-Sensing Signal DSF Inhibits LPS-Induced Inflammations by Suppressing Toll-like Receptor Signaling and Preventing Lysosome-Mediated Apoptosis in Zebrafish.International journal of molecular sciences · 2022Article
- Early-life viral infections are associated with disadvantageous immune and microbiota profiles and recurrent respiratory infections.Nature microbiology · 2022Article
- A transcriptomic analysis of the effects of macrophage polarization and endotoxin tolerance on the response to Salmonella.PloS one · 2022Article
- Congenital Infection Influence on Early Brain Development Through the Gut-Brain Axis.Frontiers in neuroscience · 2022Review
- Mechanistic and structural diversity between cytochromeProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Impact of Type I Interferons on Susceptibility to Bacterial Pathogens.Trends in microbiology · 2021Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms by which the gut luminal environment is disturbed by the immune system to foster pathogenic bacterial growth and survival remain incompletely understood. Here, we show that STAT2 dependent type I IFN signaling contributes to the inflammatory environment by disrupting hypoxia enabling the pathogenic S. Typhimurium to outgrow the microbiota. Stat2-/- mice infected with S. Typhimurium exhibited impaired type I IFN induced transcriptional responses in cecal tissue and reduced bacterial burden in the intestinal lumen compared to infected wild-type mice. Although inflammatory pathology was similar between wild-type and Stat2-/- mice, we observed decreased hypoxia in the gut tissue of Stat2-/- mice. Neutrophil numbers were similar in wild-type and Stat2-/- mice, yet Stat2-/- mice showed reduced levels of myeloperoxidase activity. In vitro, the neutrophils from Stat2-/- mice produced lower levels of superoxide anion upon stimulation with the bacterial ligand N-formylmethionyl-leucyl-phenylalanine (fMLP) in the presence of IFNα compared to neutrophils from wild-type mice, indicating that the neutrophils were less functional in Stat2-/- mice. Cytochrome bd-II oxidase-mediated respiration enhances S. Typhimurium fitness in wild-type mice, while in Stat2-/- deficiency, this respiratory pathway did not provide a fitness advantage. Furthermore, luminal expansion of S. Typhimurium in wild-type mice was blunted in Stat2-/- mice. Compared to wild-type mice which exhibited a significant perturbation in Bacteroidetes abundance, Stat2-/- mice exhibited significantly less perturbation and higher levels of Bacteroidetes upon S. Typhimurium infection. Our results highlight STAT2 dependent type I IFN mediated inflammation in the gut as a novel mechanism promoting luminal expansion of S. Typhimurium.
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