ArticleJournal of leukocyte biology2012
Slc11a1 (Nramp1) impairs growth of Salmonella enterica serovar typhimurium in macrophages via stimulation of lipocalin-2 expression.
Article in Journal of leukocyte biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 70 citations in OpenAlex.
- Review
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- Vitamin A deficiency impairs neutrophil-mediated control of Salmonella via SLC11A1 in mice.Nature microbiology · 2024Article
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- Bibliometric Review on New Possibilities of Antimycobacterial Agents: Exploring Siderophore Desferrioxamine's Applications as an Antimicrobial Agent.Pharmaceuticals (Basel, Switzerland) · 2023Review
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- A mouse model characterizes the roles of ZIP8 in systemic iron recycling and lung inflammation and infection.Blood advances · 2023Article
- Key players in the regulation of iron homeostasis at the host-pathogen interface.Frontiers in immunology · 2023Review
- Understanding How Minerals Contribute to Optimal Immune Function.Journal of immunology research · 2023Review
- Availability of Ferritin-Bound Iron to Enterobacteriaceae.International journal of molecular sciences · 2022Article
- Airway Epithelial Cells Differentially Adapt Their Iron Metabolism to Infection WithFrontiers in cellular and infection microbiology · 2022Article
- Article
- Increasing Natural Resistance Associated Macrophage Protein 1 serum level after Miana treatment in BALB/c inducedAnnals of medicine and surgery (2012) · 2021Article
- Nutritional immunity: the impact of metals on lung immune cells and the airway microbiome during chronic respiratory disease.Respiratory research · 2021Review
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The expression of the cation transporter Nramp1 (Slc11a1) in late phagolysosomes confers resistance to infection with several intracellular pathogens, such as Salmonella enterica, in mice. The antimicrobial actions of Nramp1 are attributable, in part, to modulation of macrophage immune function and cellular iron metabolism--the latter affecting the availability of the essential nutrient iron for intraphagosomal bacteria. Here, we provide novel evidence that Nramp1 functionality increases the expression of the peptide Lcn2, which exerts its antimicrobial activity by scavenging iron-loaded bacterial siderophores and mediating iron efflux from macrophages. With the use of macrophage cell lines expressing functional or nonfunctional Nramp1, we found significantly elevated Lcn2 mRNA and protein levels in Nramp1-expressing cells. These resulted from Nramp1-mediated alterations in the production of ROS, which stimulated NF-κ B activity and subsequently, Lcn2 transcription. We observed that increased Lcn2 levels in primary Nramp1-positive macrophages resulted in a significant suppression of S. enterica serovar typhimurium growth. Stimulation of Lcn2 expression is a novel mechanism by which Nramp1 confers resistance against infection with the intracellular bacterium S. typhimurium.
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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.