ArticlePloS one2012
Lipocalin 2 regulates inflammation during pulmonary mycobacterial infections.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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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Who cites it
35 citing papers in PubMed, 69 citations in OpenAlex.
- Review
- Protein Kinase C δ: a critical hub regulating macrophage immunomodulatory functions duringbioRxiv : the preprint server for biology · 2025Article
- Predictive biomarkers for latent Mycobacterium tuberculosis infection.Tuberculosis (Edinburgh, Scotland) · 2024Article
- Tolerance to Haemophilus influenzae infection in human epithelial cells: Insights from a primary cell-based model.PLoS pathogens · 2024Article
- Regulation of the innate immune response and gut microbiome by p53.Cancer science · 2024Article
- Expression Analysis of Lipocalin 2 (LCN2) in Reproductive and Non-Reproductive Tissues ofInternational journal of molecular sciences · 2023Article
- Airway epithelial cells mount an early response to mycobacterial infection.Frontiers in cellular and infection microbiology · 2023Article
- Transcriptional profiling of a fungal granuloma reveals a low metabolic activity ofFrontiers in cellular and infection microbiology · 2023Article
- Lipocalin-2 is an essential component of the innate immune response to Acinetobacter baumannii infection.PLoS pathogens · 2022Article
- IRF3 inhibits IFN-γ-mediated restriction of intracellular pathogens in macrophages independently of IFNAR.Journal of leukocyte biology · 2022Article
- Influenza A Virus Uses PSMA2 for Downregulation of the NRF2-Mediated Oxidative Stress Response.Journal of virology · 2022Article
- Airway Epithelial Cells Differentially Adapt Their Iron Metabolism to Infection WithFrontiers in cellular and infection microbiology · 2022Article
- Interplay Between the Immune and Endocrine Systems in the Lung: Implications for TB Susceptibility.Frontiers in immunology · 2022Review
- Article
- Comprehensive review of lipocalin 2-mediated effects in lung inflammation.American journal of physiology. Lung cellular and molecular physiology · 2021Review
- Lipocalin 2 regulates expression of MHC class I molecules in Mycobacterium tuberculosis-infected dendritic cells via ROS production.Cell & bioscience · 2021Article
- Inflammatory Responses of Astrocytes Are Independent from Lipocalin 2.Journal of molecular neuroscience : MN · 2021Article
- Neutrophils in Tuberculosis: Cell Biology, Cellular Networking and Multitasking in Host Defense.International journal of molecular sciences · 2021Review
- Long-term evolution of the epithelial cell secretome in preclinical 3D models of the human bronchial epithelium.Scientific reports · 2021Article
- Loss of Function of von Hippel-Lindau Trigger Lipocalin 2-Dependent Inflammatory Responses in Cultured and Primary Renal Tubular Cells.Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Pulmonary tuberculosis (TB), caused by the intracellular bacteria Mycobacterium tuberculosis, is a worldwide disease that continues to kill more than 1.5 million people every year worldwide. The accumulation of lymphocytes mediates the formation of the tubercle granuloma in the lung and is crucial for host protection against M.tuberculosis infection. However, paradoxically the tubercle granuloma is also the basis for the immunopathology associated with the disease and very little is known about the regulatory mechanisms that constrain the inflammation associated with the granulomas. Lipocalin 2 (Lcn2) is a member of the lipocalin family of proteins and binds to bacterial siderophores thereby sequestering iron required for bacterial growth. Thus far, it is not known whether Lcn2 plays a role in the inflammatory response to mycobacterial pulmonary infections. In the present study, using models of acute and chronic mycobacterial pulmonary infections, we reveal a novel role for Lcn2 in constraining T cell lymphocytic accumulation and inflammation by inhibiting inflammatory chemokines, such as CXCL9. In contrast, Lcn2 promotes neutrophil recruitment during mycobacterial pulmonary infection, by inducing G-CSF and KC in alveolar macrophages. Importantly, despite a common role for Lcn2 in regulating chemokines during mycobacterial pulmonary infections, Lcn2 deficient mice are more susceptible to acute M.bovis BCG, but not low dose M.tuberculosis pulmonary infection.
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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.