ArticleInfection and immunity1995
Growth of Mycobacterium tuberculosis in BCG-resistant and -susceptible mice: establishment of latency and reactivation.
Article in Infection and immunity, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- A Meta-analysis of MBL2 Polymorphisms and Tuberculosis Risk.Scientific reports · 2016Pooled it
- Association of MBL2 gene polymorphisms with pulmonary tuberculosis susceptibility: trial sequence meta-analysis as evidence.Infection and drug resistance · 2019Article
- Genetics of human susceptibility to active and latent tuberculosis: present knowledge and future perspectives.The Lancet. Infectious diseases · 2018Review
- Reactivation of latent tuberculosis by an inhibitor of inducible nitric oxide synthase in an aerosol murine model.Immunology · 2002Article
- Immunological and pathological comparative analysis between experimental latent tuberculous infection and progressive pulmonary tuberculosis.Clinical and experimental immunology · 2002Article
- Consequence of Nramp1 deletion to Mycobacterium tuberculosis infection in mice.Infection and immunity · 1999Article
- Granuloma formation is required to contain bacillus growth and delay mortality in mice chronically infected with Mycobacterium tuberculosis.Immunology · 1999Article
- Reactivation of tuberculosis is associated with a shift from type 1 to type 2 cytokines.Clinical and experimental immunology · 1999Article
- Cytokine production by CD4 and CD8 T cells during the growth of Mycobacterium tuberculosis in mice.Clinical and experimental immunology · 1998Article
- Phenotypic changes in T cell populations during the reactivation of tuberculosis in mice.Clinical and experimental immunology · 1998Article
- Identification of nitric oxide synthase as a protective locus against tuberculosis.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Host genetics and tuberculosis: Theory of genetic polymorphism and tuberculosis.Lung India : official organ of Indian Chest SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Growth of mycobacterial species is controlled by a gene, Bcg (candidate Nramp). Bcg acts at the macrophage level and is thought to control some aspect of macrophage priming for activation. Infection of Mycobacterium bovis BCG-susceptible (Bcgs) mice with several different mycobacterial species results in the growth of the microorganisms, while the growth of the same organisms is controlled in BCG-resistant (Bcgr) mice. The capacity of Bcg to control the growth of M. tuberculosis has not been extensively explored. The purpose of this investigation, therefore, was to compare the growth of M. tuberculosis in Bcgr and Bcgs mice. We found that the growth of tubercule bacilli was different in the lungs and spleens of Bcgr and Bcgs mice when they were inoculated with fewer then 10(3) CFU of the mycobacterium. The differences in growth were more easily distinguished in the lungs then in the spleens. The growth of the microorganisms in both strains of mice peaked between 35 and 43 days, and a latent infection was established by 65 days after infection. Activation of the hypothalamic-pituitary-adrenal axis resulted in reactivation of the growth of M. tuberculosis in both Bcgr and Bcgs mice. Greater numbers of tubercule bacilli were isolated from lungs than from spleens following reactivation. The utility of this mouse model in the study of the establishment of latency and reactivation of M. tuberculosis is discussed.
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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.