ArticleProceedings of the National Academy of Sciences of the United States of America2001
Defective localization of the NADPH phagocyte oxidase to Salmonella-containing phagosomes in tumor necrosis factor p55 receptor-deficient macrophages.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 108 citations in OpenAlex.
- The methylglyoxal pathway is a sink for glutathione in Salmonella experiencing oxidative stress.PLoS pathogens · 2023Article
- Malaria parasite infection compromises colonization resistance to an enteric pathogen by reducing gastric acidity.Science advances · 2021Article
- Proteomics of intracellular Salmonella enterica reveals roles of Salmonella pathogenicity island 2 in metabolism and antioxidant defense.PLoS pathogens · 2019Article
- Regulators of Salmonella-host interaction identified by peripheral blood transcriptome profiling: roles of TGFB1 and TRP53 in intracellular Salmonella replication in pigs.Veterinary research · 2018Article
- Effect of in vivo neutralization of tumor necrosis alpha on the efficacy of antibiotic treatment in systemic Salmonella enterica infections.Pathogens and disease · 2017Article
- Article
- Neutrophils to the ROScue: Mechanisms of NADPH Oxidase Activation and Bacterial Resistance.Frontiers in cellular and infection microbiology · 2017Review
- Genetic and Dietary Iron Overload Differentially Affect the Course ofFrontiers in cellular and infection microbiology · 2017Article
- Antioxidant Defense by Thioredoxin Can Occur Independently of Canonical Thiol-Disulfide Oxidoreductase Enzymatic Activity.Cell reports · 2016Article
- Absence of platelet endothelial cell adhesion molecule 1, PECAM-1/CD31, in vivo increases resistance to Salmonella enterica serovar Typhimurium in mice.Infection and immunity · 2013Article
- Interactions of Salmonella enterica with dendritic cells.Virulence · 2012Review
- Redox active thiol sensors of oxidative and nitrosative stress.Antioxidants & redox signaling · 2012Review
- What really happens in the neutrophil phagosome?Free radical biology & medicine · 2012Review
- Refinement of the genetics of the host response to Salmonella infection in MOLF/Ei: regulation of type 1 IFN and TRP3 pathways by Ity2.Genes and immunity · 2012Article
- Attenuated Salmonella Typhimurium lacking the pathogenicity island-2 type 3 secretion system grow to high bacterial numbers inside phagocytes in mice.PLoS pathogens · 2012Article
- Live attenuated S. Typhimurium vaccine with improved safety in immuno-compromised mice.PloS one · 2012Article
- Article
- Impact of Usp18 and IFN signaling in Salmonella-induced typhlitis.Genes and immunity · 2011Article
- Article
- The Role of the spv Genes in Salmonella Pathogenesis.Frontiers in microbiology · 2011Article
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 2 institutions in 1 country.
Funding
Abstract
Tumor necrosis factor receptor (TNFR) p55-knockout (KO) mice are susceptible profoundly to Salmonella infection. One day after peritoneal inoculation, TNFR-KO mice harbor 1,000-fold more bacteria in liver and spleen than wild-type mice despite the formation of well organized granulomas. Macrophages from TNFR-KO mice produce abundant quantities of reactive oxygen and nitrogen species in response to Salmonella but nevertheless exhibit poor bactericidal activity. Treatment with IFN-gamma enhances killing by wild-type macrophages but does not restore the killing defect of TNFR-KO cells. Bactericidal activity of macrophages can be abrogated by a deletion in the gene encoding TNFalpha but not by saturating concentrations of TNF-soluble receptor, suggesting that intracellular TNFalpha can regulate killing of Salmonella by macrophages. Peritoneal macrophages from TNFR-KO mice fail to localize NADPH oxidase-containing vesicles to Salmonella-containing vacuoles. A TNFR-KO mutation substantially restores virulence to an attenuated mutant bacterial strain lacking the type III secretory system encoded by Salmonella pathogenicity island 2 (SPI2), suggesting that TNFalpha and SPI2 have opposing actions on a common pathway of vesicular trafficking. TNFalpha-TNFRp55 signaling plays a critical role in the immediate innate immune response to an intracellular pathogen by optimizing the delivery of toxic reactive oxygen species to the phagosome.
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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.