Evidence map›Paper›PMID 10209511›Full record

ArticleClinical and experimental immunology1999

Apoptosis of Mycobacterium avium-infected macrophages is mediated by both tumour necrosis factor (TNF) and Fas, and involves the activation of caspases.

L E Bermudez, A Parker, M Petrofsky

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Clinical and experimental immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Cell death pathways in response toInfection and immunity · 2025
    Review
  2. Article
  3. Microorganisms · 2022
    Review
  4. Genetic Involvement ofInternational journal of molecular sciences · 2021
    Review
  5. Article
  6. TNFR1 and TNFR2 in the Control of the Life and Death Balance of Macrophages.Frontiers in cell and developmental biology · 2019
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Identification of Mycobacterium avium pathogenicity island important for macrophage and amoeba infection.Proceedings of the National Academy of Sciences of the United States of America · 2007
    Article
  17. Whipple's disease: a macrophage disease.Clinical and vaccine immunology : CVI · 2006
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

L E BermudezKuzell Institute for Arthritis and Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco 94115, USA. luizb@cooper.cmpc.org
A Parker
M Petrofsky
California Pacific Medical Center · US

Funding

EVALUATION OF THERAPIES FOR MYOBACTERIUM AVIUMN01AI025140 · NIAID · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI YOUNG, LOWELL S. · 1992 to 1998
–
PATHOGENESIS &HOST DEFENSE AGAINST M. AVIUMR01AI025769 · NIAID · MEDICAL RESEARCH INSTITUTE OF SAN FRAN · PI YOUNG, LOWELL S. · 1987 to 1994
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NIAID NIH HHS AI-25769NIAID NIH HHS N01-AI-25140
6 · The paper itself

Abstract

Mycobacterium avium causes disseminated infection in AIDS patients and several forms of infection in immunocompetent hosts. Recent studies have shown that M. avium infection of macrophages in vitro leads to apoptosis of significant numbers of infected cells. Several strains of M. avium used to infect human macrophages for 5 days (multiplicity of infection of 10) triggered 28-46% higher levels of apoptosis than observed with uninfected macrophages at the same time points. Mycobacterium avium strains unable to replicate intracellularly (rep-) resulted in a 15% rate of apoptosis, while M. smegmatis-infected monolayers showed the same percentage of apoptotic cells as the uninfected macrophage control. The presence of anti-TNF-alpha antibody reduced apoptosis to 17% and the presence of anti-Fas antibody reduced apoptosis to 10%. When both antibodies were used together, the apoptosis level was 5% above the control. Treatment with TGF-beta also reduced the number of apoptotic cells in infected monolayers. If intracellular growth was inhibited, apoptosis of macrophages decreased significantly. It was also shown that apoptosis was associated with IL-1 beta-converting enzyme (ICE) activation and was significantly reduced by a caspase inhibitor. Gaining understanding of the mechanisms of M. avium-associated apoptosis of macrophages will provide important insight into M. avium pathogenesis.

Indexed as

ApoptosisCaspase 1Caspase InhibitorsCaspasesEnzyme Activationfas ReceptorHumansMacrophagesMycobacterium aviumMycobacterium smegmatisSignal TransductionTumor Necrosis Factor-alphaCaspase 1Caspase InhibitorsCaspasesfas ReceptorTumor Necrosis Factor-alpha

Identifiers

PMID10209511
PMCPMC1905226
OpenAlexW1607217270

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.