Evidence map›Paper›PMID 9125580›Full record

ArticleInfection and immunity1997

Growth within macrophages increases the efficiency of Mycobacterium avium in invading other macrophages by a complement receptor-independent pathway.

L E Bermudez, A Parker, J R Goodman

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 89 citations in OpenAlex.

  1. TheMicroorganisms · 2025
    Review
  2. Article
  3. Genetic Involvement ofInternational journal of molecular sciences · 2021
    Review
  4. Roles of EvpP inFrontiers in cellular and infection microbiology · 2020
    Article
  5. PPE38 Protein ofFrontiers in cellular and infection microbiology · 2017
    Article
  6. Article
  7. Analysis of Ebola Virus Entry Into Macrophages.The Journal of infectious diseases · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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 of Arthritis and Infectious Diseases, California Pacific Medical Center Research Institute, San Francisco 94115, USA.
A Parker
J R Goodman
California Pacific Medical Center · US

Funding

PATHOGENESIS &HOST DEFENSE AGAINST M. AVIUMR01AI025769 · NIAID · MEDICAL RESEARCH INSTITUTE OF SAN FRAN · PI YOUNG, LOWELL S. · 1987 to 1994
–
NIAID NIH HHS AI 25769
6 · The paper itself

Abstract

Infections caused by organisms of the Mycobacterium avium complex occur in approximately 50 to 60% of patients with AIDS. M. avium is an intracellular pathogen that survives and multiplies within mononuclear phagocytes. In this study, we investigated the uptake of M. avium grown within macrophages (intracellular growth M. avium [IG]) by a second macrophage compared with M. avium cultured in broth (extracellular growth M. avium [EG]). The results showed that IG was six- to eightfold more efficient than EG in entering macrophages. In addition, while an anti-CR3 antibody was able to inhibit approximately 60% of EG uptake by macrophages, it failed to inhibit the entry of IG. In contrast to EG, IG uptake into macrophages was significantly inhibited in the presence of anti-beta1-integrin and anti-transferrin receptor antibodies. Entry into macrophages by alternate receptors was associated with resistance to tumor necrosis factor alpha (TNF-alpha) stimulation. While stimulation with TNF-alpha resulted in inhibition of the growth of EG, it was not associated with inhibition of intracellular growth of IG. Investigation of the reason why M. avium is able to sense the changes in the intracellular environment triggering a change to the invasive phenotype suggests a direct relationship with macrophage apoptosis. These results suggest that intracellular growth is associated with novel mechanisms of M. avium uptake of macrophages and that those mechanisms appear to offer advantages to the bacteria in escaping the host defense.

Indexed as

Antibodies, BlockingApoptosisCatalaseCulture MediaDextran SulfateDNA FragmentationHeparinHumansIntegrin beta1Macrophage-1 AntigenMacrophagesMicroscopy, ElectronMycobacterium avium ComplexMycobacterium avium-intracellulare InfectionPhagocytosisPolysaccharidesAntibodies, BlockingCatalaseCulture MediaDextran SulfatefucoidanHeparinIntegrin beta1Macrophage-1 AntigenPolysaccharidesReceptors, TransferrinTumor Necrosis Factor-alpha

Identifiers

PMID9125580
PMCPMC175241
OpenAlexW2171442823

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.