ArticleJournal of innate immunity2013
Mycobacterium tuberculosis- induced neutrophil extracellular traps activate human macrophages.
Article in Journal of innate immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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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
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- In vitro induction of NETosis: Comprehensive live imaging comparison and systematic review.PloS one · 2017Pooled it
- Nano-NucleOTAC-mediated Z-DNA transformation disrupts mycobacterium tuberculosis biofilms and activates antibacterial immunity.Nature communications · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Neutrophil Extracellular Trap Formation-Derived Peptidylarginine Deiminases in the Citrullination of Oral Bacteria to Promote Inflammation in Rheumatoid Arthritis.The Journal of rheumatology · 2026Article
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- NETosis associates with human TB lung tissue destruction and disease pathogenesis.EMBO molecular medicine · 2026Article
- Ischaemia in tuberculous meningitis: update on pathophysiology, clinical predictors and management.Current opinion in infectious diseases · 2026Review
- The Emerging Role of Immunothrombosis in the Control and Pathogenesis of Mycobacterium tuberculosis.The Journal of infectious diseases · 2026Review
- Immunotherapy for tuberculosis: current landscape, mechanistic insights, and translational perspectives.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in gynecological disease: pathogenic mechanisms and therapeutic opportunities.Frontiers in medicine · 2026Review
- Differential Neutrophil Responses to Smooth Titanium: A Double-Edged Sword for the Abutment-Gingival Interface (An In Vitro Study).International journal of dentistry · 2026Article
- Neutrophil extracellular traps in diabetic wound healing: mechanisms, pathological roles, and therapeutic implications.Burns & trauma · 2026Review
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- Mechanisms and immune crosstalk of neutrophil extracellular traps in response to infection.mBio · 2025Review
- Article
- A Mimetic Assay of Neutrophil Extracellular Trap Degradation Using YOYO-1-Stained DNA-Histone Surface Webs.Cells · 2025Article
- Host Immune Response toJournal of inflammation research · 2025Review
- Machine learning-driven discovery of NETs-associated diagnostic biomarkers and molecular subtypes in tuberculosis.Frontiers in cellular and infection microbiology · 2025Article
- Where lung cancer and tuberculosis intersect: recent advances.Frontiers in immunology · 2025Review
- Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation.Cell host & microbe · 2024Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils activated by Mycobacterium tuberculosis (Mtb) form neutrophil extracellular traps (NETs), containing DNA and several biologically active cytosolic and granular proteins. These NETs may assist in the innate immune defense against different pathogens. We investigated whether the NET-forming neutrophils mediate an activating signal to macrophages during the early multicellular inflammatory reaction and granuloma formation. Mtb-induced NETs were found to be reactive oxygen species dependent and phagocytosis dependent. A neutrophil elastase inhibitor also delayed NET formation. However, NET formation occurred independently of Mtb-induced apoptosis. We observed close interactions between macrophages and Mtb-activated neutrophils, where macrophages bound and phagocytosed NETs. Significant secretion of the cytokines interleukin (IL)-6, tumor necrosis factor-α, IL-1β and IL-10 were detected from macrophages cocultured with NETs from Mtb-activated but not phorbol myristate acetate-activated neutrophils. NETs binding heat shock protein 72 (Hsp72) or recombinant Hsp72 were able to trigger cytokine release from macrophages. Only Mtb-induced NETs contained Hsp72, suggesting that these NETs can transfer this danger signal to adjacent macrophages. We propose that Hsp72 sequestered in NETs plays an important role in the interaction between neutrophils and macrophages during the early innate immune phase of an Mtb infection. The immunomodulatory role of NETs and proteins derived from them may influence not only chronic inflammation during tuberculosis but also immune regulation and autoimmunity.
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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.