ArticlePLoS pathogens2017
Innate activation of human primary epithelial cells broadens the host response to Mycobacterium tuberculosis in the airways.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 69 citations in OpenAlex.
- Probing Dermal Immunity to Mycobacteria through a Controlled Human Infection Model.ImmunoHorizons · 2024Trial
- Lung organoids as a human system for Mycobacteria infection modeling and drug testing.The FEBS journal · 2026Review
- Article
- Structural and Functional Characterization of Protein Adhesins and Pili in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Article
- Prior Exposure of Airway Epithelial Cells to Mycobacteria Reduces Subsequent <italic>Mycobacterium tuberculosis</italic> Infection and Resulting Inflammation.Journal of innate immunity · 2026Article
- RBMX2 linkseLife · 2025Article
- Lung epithelial injury impairs early host immune responses to Mycobacterium tuberculosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Article
- In vitro modelling of bacterial pneumonia: a comparative analysis of widely applied complex cell culture models.FEMS microbiology reviews · 2024Review
- The uncharted territory of host-pathogen interaction in tuberculosis.Frontiers in immunology · 2024Review
- Protective interplay:Frontiers in immunology · 2024Article
- Dual oxidase 1 is dispensable duringFrontiers in immunology · 2023Article
- Initial immune response after exposure toFrontiers in immunology · 2023Review
- Airway epithelial cells mount an early response to mycobacterial infection.Frontiers in cellular and infection microbiology · 2023Article
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- 3D Human Organoids: The Next "Viral" Model for the Molecular Basis of Infectious Diseases.Biomedicines · 2022Review
- Estradiol inhibits autophagy ofMolecular medicine reports · 2022Article
- Lung epithelial cells interact with immune cells and bacteria to shape the microenvironment in tuberculosis.Thorax · 2022Review
- Mycobacteria-host interactions in human bronchiolar airway organoids.Molecular microbiology · 2022Article
- Microbiome-immune interactions in tuberculosis.PLoS pathogens · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Early events in the human airways determining whether exposure to Mycobacterium tuberculosis (Mtb) results in acquisition of infection are poorly understood. Epithelial cells are the dominant cell type in the lungs, but little is known about their role in tuberculosis. We hypothesised that human primary airway epithelial cells are part of the first line of defense against Mtb-infection and contribute to the protective host response in the human respiratory tract. We modelled these early airway-interactions with human primary bronchial epithelial cells (PBECs) and alveolar macrophages. By combining in vitro infection and transwell co-culture models with a global transcriptomic approach, we identified PBECs to be inert to direct Mtb-infection, yet to be potent responders within an Mtb-activated immune network, mediated by IL1β and type I interferon (IFN). Activation of PBECs by Mtb-infected alveolar macrophages and monocytes increased expression of known and novel antimycobacterial peptides, defensins and S100-family members and epithelial-myeloid interactions further shaped the immunological environment during Mtb-infection by promoting neutrophil influx. This is the first in depth analysis of the primary epithelial response to infection and offers new insights into their emerging role in tuberculosis through complementing and amplifying responses to Mtb.
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.