ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Impaired neutrophil function in 24p3 null mice contributes to enhanced susceptibility to bacterial infections.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- Epigenetic regulation of neutrophil dysfunction in sepsis: mechanisms, biomarkers, and translational challenges.Journal of translational medicine · 2026Review
- IL-6 trans-Signaling Regulates Neutrophilic Inflammation in Alcohol-Associated Hepatitis.The American journal of pathology · 2026Article
- Serum neutrophil gelatinase associated Lipocalin as a novel biomarker for diagnosing acute pyelonephritis in adults.Scientific reports · 2025Article
- ComplexEye: a multi-lens array microscope for high-throughput embedded immune cell migration analysis.Nature communications · 2023Article
- The Review of Current Knowledge on Neutrophil Gelatinase-Associated Lipocalin (NGAL).International journal of molecular sciences · 2023Review
- Lipocalin family proteins and their diverse roles in cardiovascular disease.Pharmacology & therapeutics · 2023Review
- Article
- Understanding How Minerals Contribute to Optimal Immune Function.Journal of immunology research · 2023Review
- Lipocalin 2 regulates expression of MHC class I molecules in Mycobacterium tuberculosis-infected dendritic cells via ROS production.Cell & bioscience · 2021Article
- Lipocalin-2 Alleviates LPS-Induced Inflammation Through Alteration of Macrophage Properties.Journal of inflammation research · 2021Article
- Plasma Lipocalin-2 and Adiponectin are Affected by Obesity Rather Than Type 2 Diabetes Mellitus per se.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Lipocalin 2 Is a Regulator During Macrophage Polarization Induced by Soluble Worm Antigens.Frontiers in cellular and infection microbiology · 2021Article
- Advances in the In Vivo Molecular Imaging of Invasive Aspergillosis.Journal of fungi (Basel, Switzerland) · 2020Review
- Macrophage-Derived Iron-Bound Lipocalin-2 Correlates with Renal Recovery Markers Following Sepsis-Induced Kidney Damage.International journal of molecular sciences · 2020Article
- Functions and regulation of lipocalin-2 in gut-origin sepsis: a narrative review.Critical care (London, England) · 2019Review
- Iron as a Central Player and Promising Target in Cancer Progression.International journal of molecular sciences · 2019Review
- Diet-Microbe-Host Interactions That Affect Gut Mucosal Integrity and Infection Resistance.Frontiers in immunology · 2019Review
- The Pivotal Role of Regulatory T Cells in the Regulation of Innate Immune Cells.Frontiers in immunology · 2019Review
- Lipocalin 24p3 Induction in Colitis Adversely Affects Inflammation and Contributes to Mortality.Frontiers in immunology · 2019Article
- Lipocalin 2 Protects AgainstFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Lipocalin 24p3 (24p3) is a neutrophil secondary granule protein. 24p3 is also a siderocalin, which binds several bacterial siderophores. It was therefore proposed that synthesis and secretion of 24p3 by stimulated macrophages or release of 24p3 upon neutrophil degranulation sequesters iron-laden siderophores to attenuate bacterial growth. Accordingly, 24p3-deficient mice are susceptible to bacterial pathogens for which siderophores would normally be chelated by 24p3. Specific granule deficiency (SGD) is a rare congenital disorder characterized by complete absence of proteins in secondary granules. Neutrophils from SGD patients, who are prone to bacterial infections, lack normal functions, but the potential role of 24p3 in neutrophil dysfunction in SGD is not known. In this study, we show that neutrophils from mice genetically deficient for lipocalin 24p3 (24p3(-/-)) are defective in many neutrophil functions. Specifically, neutrophils in 24p3(-/-) mice do not extravasate to sites of infection and are defective for chemotaxis. A transcriptome analysis revealed that genes that control cytoskeletal reorganization are selectively suppressed in 24p3(-/-) neutrophils. Additionally, small regulatory RNAs (microRNAs) that control upstream regulators of cytoskeletal proteins are also increased in 24p3(-/-) neutrophils. Further, 24p3(-/-) neutrophils failed to phagocytose bacteria, which may account for the enhanced sensitivity of 24p3(-/-) mice to both intracellular (Listeria monocytogenes) and extracellular (Candida albicans and Staphylococcus aureus) pathogens. Listeria does not secrete siderophores, and additionally, the siderophore secreted by Candida is not sequestered by 24p3. Therefore, the heightened sensitivity of 24p3(-/-) mice to these pathogens is not due to sequestration of siderophores limiting iron availability, but is a consequence of impaired neutrophil function.
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Registered trials
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