ArticleMolecular microbiology2010
Potential role for ESAT6 in dissemination of M. tuberculosis via human lung epithelial cells.
Article in Molecular microbiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 119 citations in OpenAlex.
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- Structural and Functional Characterization of Protein Adhesins and Pili in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Article
- Stopping Tuberculosis at the Gate: The Role ofVaccines · 2025Review
- Metabolically active neutrophils represent a permissive niche for Mycobacterium tuberculosis.Mucosal immunology · 2024Article
- ESAT-6 undergoes self-association at phagosomal pH and an ESAT-6-specific nanobody restrictseLife · 2024Article
- Serine protease Rv2569c facilitates transmission of Mycobacterium tuberculosis via disrupting the epithelial barrier by cleaving E-cadherin.PLoS pathogens · 2024Article
- ESAT-6 undergoes self-association at phagosomal pH and an ESAT-6 specific nanobody restricts M. tuberculosis growth in macrophages.bioRxiv : the preprint server for biology · 2024Article
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Pathogenicity and virulence ofVirulence · 2023Review
- Uptake-independent killing of macrophages by extracellular Mycobacterium tuberculosis aggregates.The EMBO journal · 2023Article
- An N-acetyltransferase required for EsxA N-terminal protein acetylation and virulence in Mycobacterium marinum.bioRxiv : the preprint server for biology · 2023Article
- Early innate cell interactions withFrontiers in immunology · 2023Review
- Novel intravesical bacterial immunotherapy induces rejection of BCG-unresponsive established bladder tumors.Journal for immunotherapy of cancer · 2022Article
- N-terminal signal peptides facilitate the engineering of PVC complex as a potent protein delivery system.Science advances · 2022Article
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- A Small Protein but with Diverse Roles: A Review of EsxA in Mycobacterium-Host Interaction.Cells · 2021Review
- In Vitro Models for Studying Respiratory Host-Pathogen Interactions.Advanced biology · 2021Review
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- Alginate-Capped Silver Nanoparticles as a Potent Anti-mycobacterial Agent AgainstFrontiers in pharmacology · 2021Article
6 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
9 authors at 4 institutions in 3 countries.
Funding
Abstract
ESAT6 has recently been demonstrated to cause haemolysis and macrophage lysis. Our studies demonstrate that ESAT6 causes cytolysis of type 1 and type 2 pneumocytes. Both types of pneumocytes express membrane laminin, and ESAT6 exhibits dose-dependent binding to both cell types and to purified human laminin. While minimal ESAT6 was detected on the surface of Mycobacterium tuberculosis grown in vitro, exogenously provided ESAT6 specifically associated with the bacterial cell surface, and the bacterium-associated ESAT6 retained its cytolytic ability. esat6 transcripts were upregulated approximately 4- to approximately 13-fold in bacteria replicating in type 1 cells, and approximately 3- to approximately 5 fold in type 2 cells. In vivo, laminin is primarily concentrated at the basolateral surface of pneumocytes where they rest on the basement membrane, which is composed primarily of laminin and collagen. The upregulation of esat6 transcripts in bacteria replicating in pneumocytes, the specific association of ESAT6 with the bacterial surface, the binding of ESAT6 to laminin and the lysis of pneumocytes by free and bacterium-associated ESAT6 together suggest a scenario wherein Mycobacterium tuberculosis replicating in pneumocytes may utilize surface ESAT6 to anchor onto the basolateral laminin-expressing surface of the pneumocytes, and damage the cells and the basement membrane to directly disseminate through the alveolar wall.
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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.