ArticleInfection and immunity2000
Necrosis of lung epithelial cells during infection with Mycobacterium tuberculosis is preceded by cell permeation.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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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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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.
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Who cites it
54 citing papers in PubMed, 108 citations in OpenAlex.
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- Mycobacterium tuberculosis curli pili (MTP) facilitates pathogenicity by modulating oxidative phosphorylation and carbon flux during early infection of A549 epithelial cells.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
- Role of C-terminal domain of Mycobacterium tuberculosis PE6 (Rv0335c) protein in host mitochondrial stress and macrophage apoptosis.Apoptosis : an international journal on programmed cell death · 2023Article
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
- A Small Protein but with Diverse Roles: A Review of EsxA in Mycobacterium-Host Interaction.Cells · 2021Review
- From infection niche to therapeutic target: the intracellular lifestyle ofMicrobiology (Reading, England) · 2021Review
- Role of Extracellular Mycobacteria in Blood-Retinal Barrier Invasion in a Zebrafish Model of Ocular TB.Pathogens (Basel, Switzerland) · 2021Article
- Mesenchymal Stem Cells and Tuberculosis: Clinical Challenges and Opportunities.Frontiers in immunology · 2021Review
- Modeling Tubercular ESX-1 Secretion Using Mycobacterium marinum.Microbiology and molecular biology reviews : MMBR · 2020Review
- Modelling early events in Mycobacterium bovis infection using a co-culture model of the bovine alveolus.Scientific reports · 2020Article
- Mycobacterium tuberculosis curli pili (MTP) is associated with significant host metabolic pathways in an A549 epithelial cell infection model and contributes to the pathogenicity of Mycobacterium tuberculosis.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- Article
- Mycobacterial Control of Host Mitochondria: Bioenergetic and Metabolic Changes Shaping Cell Fate and Infection Outcome.Frontiers in cellular and infection microbiology · 2020Review
- Infect and Inject: HowMicrobiology spectrum · 2019Review
- Infection resisters: targets of new research for uncovering natural protective immunity againstF1000Research · 2019Review
- Review
- Transcriptional Profile ofFrontiers in cellular and infection microbiology · 2018Article
- Necrosis Driven Triglyceride Synthesis Primes Macrophages for Inflammation DuringFrontiers in 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mycobacterium tuberculosis establishes infection, progresses towards disease, and is transmitted from the alveolus of the lung. However, the role of the alveolar epithelium in any of these pathogenic processes of tuberculosis is unclear. In this study, lung epithelial cells (A549) were used as a model in which to examine cytotoxicity during infection with either virulent or avirulent mycobacteria in order to further establish the role of the lung epithelium during tuberculosis. Infection of A549 cells with M. tuberculosis strains Erdman and CDC1551 demonstrated significant cell monolayer clearing, whereas infection with either Mycobacterium bovis BCG or Mycobacterium smegmatis LR222 did not. Clearing of M. tuberculosis-infected A549 cells correlated to necrosis, not apoptosis. Treatment of M. tuberculosis-infected A549 cells with streptomycin, but not cycloheximide, demonstrated a significant reduction in the necrosis of A549 cell monolayers. This mycobacterium-induced A549 necrosis did not correlate to higher levels of intracellular or extracellular growth by the mycobacteria during infection. Staining of infected cells with propidium iodide demonstrated that M. tuberculosis induced increased permeation of A549 cell membranes within 24 h postinfection. Quantitation of lactate dehydrogenase (LDH) release from infected cells further demonstrated that cell permeation was specific to M. tuberculosis infection and correlated to A549 cellular necrosis. Inactivated M. tuberculosis or its subcellular fractions did not result in A549 necrosis or LDH release. These studies demonstrate that lung epithelial cell cytotoxicity is specific to infection by virulent mycobacteria and is caused by cellular necrosis. This necrosis is not a direct correlate of mycobacterial growth or of the expression of host cell factors, but is preceded by permeation of the A549 cell membrane and requires infection with live bacilli.
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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.