ArticleThe Journal of infectious diseases2015
Lung Mucosa Lining Fluid Modification of Mycobacterium tuberculosis to Reprogram Human Neutrophil Killing Mechanisms.
Article in The Journal of infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Neutrophils and tuberculosis - insights into immunobiology and pathogenesis.Molecular biology reports · 2026Review
- Identification and validation of NETs-related biomarkers in active tuberculosis through bioinformatics analysis and machine learning algorithms.Frontiers in immunology · 2025Article
- HIV infection impairs the host response to Mycobacterium tuberculosis infection by altering surfactant protein D function in the human lung alveolar mucosa.Mucosal immunology · 2024Article
- Human alveolar lining fluid from the elderly promotes Mycobacterium tuberculosis intracellular growth and translocation into the cytosol of alveolar epithelial cells.Mucosal immunology · 2024Article
- Challenges in Developing a Controlled Human Tuberculosis Challenge Model.Current topics in microbiology and immunology · 2024Review
- Exposure ofFrontiers in tuberculosis · 2024Article
- Review
- Tuberculosis in an Aging World.Pathogens (Basel, Switzerland) · 2022Review
- Host- and Age-Dependent Transcriptional Changes inInternational journal of molecular sciences · 2022Article
- The Impact of Aging on the Lung Alveolar Environment, Predetermining Susceptibility to Respiratory Infections.Frontiers in aging · 2022Review
- Role of Extracellular Trap Release During Bacterial and Viral Infection.Frontiers in microbiology · 2022Review
- Neutrophils in Tuberculosis: Cell Biology, Cellular Networking and Multitasking in Host Defense.International journal of molecular sciences · 2021Review
- Evolution of Drug-ResistantFrontiers in microbiology · 2021Review
- Antimicrobial Activity of Neutrophils Against Mycobacteria.Frontiers in immunology · 2021Review
- Host defense mechanisms against Mycobacterium tuberculosis.Cellular and molecular life sciences : CMLS · 2020Review
- Formation of Lung Inducible Bronchus Associated Lymphoid Tissue Is Regulated byFrontiers in immunology · 2020Article
- The Lung Mucosa Environment in the Elderly Increases Host Susceptibility to Mycobacterium tuberculosis Infection.The Journal of infectious diseases · 2019Article
- Underestimated Manipulative Roles ofFrontiers in immunology · 2019Review
- Mannose-capped lipoarabinomannan in Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- Exposure to human alveolar lining fluid enhances Mycobacterium bovis BCG vaccine efficacy against Mycobacterium tuberculosis infection in a CD8Mucosal immunology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We have shown that human alveolar lining fluid (ALF) contains homeostatic hydrolases capable of altering the Mycobacterium tuberculosis cell wall and subsequently its interaction with human macrophages. Neutrophils are also an integral part of the host immune response to M. tuberculosis infection. Here we show that the human lung mucosa influences M. tuberculosis interaction with neutrophils, enhancing the intracellular killing of ALF-exposed M. tuberculosis and up-regulating the expression of tumor necrosis factor and interleukin 8. In contrast, ALF-exposed M. tuberculosis does not induce neutrophil apoptosis or necrosis, degranulation, or release of extracellular traps, and it decreases the oxidative response. These results suggest an important role for the human alveolar mucosa: increasing the innate capacity of the neutrophil to recognize and kill M. tuberculosis by favoring the use of intracellular mechanisms, while at the same time limiting neutrophil extracellular inflammatory responses to minimize their associated tissue damage.
Indexed as
Identifiers
What OpenQuestion holds
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.