ReviewPathogens (Basel, Switzerland)2018
Pathogenesis and Animal Models of Post-Primary (Bronchogenic) Tuberculosis, A Review.
Review in Pathogens (Basel, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 40 citations in OpenAlex.
- Radiological and functional evidence of the bronchial spread of tuberculosis: an observational analysis.The Lancet. Microbe · 2021Trial
- Sertraline Enhances Bacterial Control without Adversely Affecting the Pharmacodynamic-Pharmacokinetic Properties of Frontline Tuberculosis Drugs.ACS pharmacology & translational science · 2026Article
- Deciphering the Molecular Interactions of Tuberculosis and Colorectal Cancer: A Network and RNA-Seq Data Analysis Approach.Anti-cancer agents in medicinal chemistry · 2026Article
- Distinct clinical outcomes in pediatric tuberculosis: A study utilizing infant macaques exposed to aerosoliScience · 2025Article
- Host Immune Response toJournal of inflammation research · 2025Review
- Article
- Article
- A Novel Humanized Mouse Model for HIV and Tuberculosis Co-infection Studies.bioRxiv : the preprint server for biology · 2024Article
- A novel humanized mouse model for HIV and tuberculosis co-infection studies.Frontiers in immunology · 2024Article
- Understanding the development of tuberculous granulomas: insights into host protection and pathogenesis, a review in humans and animals.Frontiers in immunology · 2024Review
- Novel Insights into the Pathogenesis of Human Post-Primary Tuberculosis from Archival Material of the Pre-Antibiotic Era, 1931-1947.Pathogens (Basel, Switzerland) · 2023Article
- Clinical manifestations and immune response to tuberculosis.World journal of microbiology & biotechnology · 2023Review
- Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023Review
- Specific identification ofMethodsX · 2023Article
- The paradox of immune checkpoint inhibition re-activating tuberculosis.The European respiratory journal · 2022Review
- Immunologic and imaging signatures in post tuberculosis lung disease.Tuberculosis (Edinburgh, Scotland) · 2022Review
- Review
- In the Thick of It: Formation of the Tuberculous Granuloma and Its Effects on Host and Therapeutic Responses.Frontiers in immunology · 2022Review
- A Ginger Root or Plum Model for the Tuberculosis "Granuloma"?American journal of respiratory and critical care medicine · 2021Article
- Vaccination with BCGΔBCG1419c protects against pulmonary and extrapulmonary TB and is safer than BCG.Scientific reports · 2021Article
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 3 institutions in 1 country.
Funding
Abstract
Primary and post-primary tuberculosis (TB) are different diseases caused by the same organism. Primary TB produces systemic immunity. Post-primary TB produces cavities to support massive proliferation of organisms for transmission of infection to new hosts from a person with sufficient immunity to prevent systemic infection. Post-primary, also known as bronchogenic, TB begins in humans as asymptomatic bronchial spread of obstructive lobular pneumonia, not as expanding granulomas. Most lesions regress spontaneously. However, some undergo caseation necrosis that is coughed out through the necrotic bronchi to form cavities. Caseous pneumonia that is not expelled through the bronchi is retained to become the focus of fibrocaseous disease. No animal reproduces this entire process. However, it appears that many mammals utilize similar mechanisms, but fail to coordinate them as do humans. Understanding this makes it possible to use human tuberculous lung sections to guide manipulation of animals to produce models of particular human lesions. For example, slowly progressive and reactivation TB in mice resemble developing human bronchogenic TB. Similarly, bronchogenic TB and cavities resembling those in humans can be induced by bronchial infection of sensitized rabbits. Granulomas in guinea pigs have characteristics of both primary and post primary TB. Mice can be induced to produce a spectrum of human like caseating granulomas. There is evidence that primates can develop bronchogenic TB. We are optimistic that such models developed by coordinated study of human and animal tissues can be used with modern technologies to finally address long-standing questions about host/parasite relationships in TB, and support development of targeted therapeutics and vaccines.
Indexed as
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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.