ArticleTuberculosis (Edinburgh, Scotland)2014
A new unifying theory of the pathogenesis of tuberculosis.
Article in Tuberculosis (Edinburgh, Scotland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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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.
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.
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Who cites it
64 citing papers in PubMed, 138 citations in OpenAlex.
- Tissue-resident-like CD4+ T cells secreting IL-17 control Mycobacterium tuberculosis in the human lung.The Journal of clinical investigation · 2021Trial
- The Synergistic Effects of the Glutathione Precursor, NAC and First-Line Antibiotics in the Granulomatous Response AgainstFrontiers in immunology · 2018Trial
- Design of a multi-epitope vaccine against Mycobacterium tuberculosis using reverse vaccinology and immunoreactive peptides.Genomics & informatics · 2026Article
- Application of luminescence-producing Mycobacterium tuberculosis strains for evaluating anti-tuberculosis drug and vaccine efficacy in vitro and in vivo.BMC infectious diseases · 2026Article
- The role of neutrophil response in lung damage and post-tuberculosis lung disease: a translational narrative review.Frontiers in immunology · 2025Review
- Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation.Cell host & microbe · 2024Article
- Cellulase Promotes Mycobacterial Biofilm Dispersal in Response to a Decrease in the Bacterial Metabolite Gamma-Aminobutyric Acid.International journal of molecular sciences · 2024Article
- Review
- Uptake-independent killing of macrophages by extracellular Mycobacterium tuberculosis aggregates.The EMBO journal · 2023Article
- Polyphosphate kinase 1 is involved in formation, the morphology and ultramicrostructure of biofilm ofHeliyon · 2023Article
- The functional response of human monocyte-derived macrophages to serum amyloid A andFrontiers in immunology · 2023Article
- Bacterial biofilms in the human body: prevalence and impacts on health and disease.Frontiers in cellular and infection microbiology · 2023Review
- Review
- In vitro anti-tuberculosis effect of probiotic Lacticaseibacillus rhamnosus PMC203 isolated from vaginal microbiota.Scientific reports · 2022Article
- PE_PGRS3 ensures provision of the vital phospholipids cardiolipin and phosphatidylinositols by promoting the interaction betweenVirulence · 2021Article
- Vaccination with BCGΔBCG1419c protects against pulmonary and extrapulmonary TB and is safer than BCG.Scientific reports · 2021Article
- Article
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- AggregatedFrontiers in microbiology · 2021Article
- Lactate Metabolism and Signaling in Tuberculosis and Cancer: A Comparative Review.Frontiers in cellular and infection microbiology · 2021Review
4 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
1 author at 1 institution in 1 country.
Funding
Abstract
It is set in stone that Mycobacterium tuberculosis is a facultative intracellular bacterial parasite. This axiom drives our knowledge of the host response, the way we design vaccines against the organism by generating protective T cells, and to a lesser extent, the way we try to target anti-microbial drugs. The purpose of this article is to commit total heresy. I believe that M. tuberculosis can equally well be regarded as an extracellular pathogen and may in fact spend a large percentage of its human lung "life-cycle" in this environment. It is of course intracellular as well, but this may well be little more than a brief interlude after infection of a new host during which the bacterium must replicate to increase its chances of transmission and physiologically adapt prior to moving back to an extracellular phase. As a result, by focusing almost completely on just the intracellular phase, we may be making serious strategic errors in the way we try to intervene in this pathogenic process. It is my opinion that when a TB bacillus enters the lungs and starts to reside inside an alveolar macrophage, its central driving force is to switch on a process leading to lung necrosis, since it is only by this process that the local lung tissue can be destroyed and the bacillus can be exhaled and transmitted. I present here a new model of the pathogenesis of the disease that attempts to unify the pathogenic process of infection, disease, persistence [rather than latency], and reactivation.
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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.