Evidence map›Paper›PMID 2826638›Full record

ArticleThe Journal of experimental medicine1988

The effect of phenolic glycolipid-1 from Mycobacterium leprae on the antimicrobial activity of human macrophages.

M A Neill, S J Klebanoff

Open access · greenAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
  2. Cell Biology of Intracellular Adaptation ofMicrobiology spectrum · 2019
    Review
  3. Article
  4. Article
  5. Article
  6. Modulation of the cytokine response in human monocytes by mycobacterium leprae phenolic glycolipid-1.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2012
    Article
  7. Article
  8. Article
  9. Article
  10. MmpL8 is required for sulfolipid-1 biosynthesis and Mycobacterium tuberculosis virulence.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  11. Article
  12. Innate immunity to Mycobacterium tuberculosis.Clinical microbiology reviews · 2002
    Review
  13. Article
  14. Article
  15. A novel antioxidant gene from Mycobacterium tuberculosis.The Journal of experimental medicine · 1997
    Article
  16. Article
  17. Role of oxidants in microbial pathophysiology.Clinical microbiology reviews · 1997
    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

2 authors at 1 institution in 1 country.

M A NeillDepartment of Medicine, University of Washington, Seattle 98195.
S J Klebanoff
University of Washington · US

Funding

ANTIMICROBIAL EFFECT OF PEROXIDASE - ROLE IN LEUKOCYTESR01AI007763 · NIAID · UNIVERSITY OF WASHINGTON · PI KLEBANOFF, SEYMOUR J · 1985 to 1987
–
ANTIMICROBIAL EFFECT OF PEROXIDASE--ROLE IN LEUKOCYTESR37AI007763 · NIAID · UNIVERSITY OF WASHINGTON · PI KLEBANOFF, SEYMOUR J · 1988 to 1999
–
NIAID NIH HHS AI-O7763
6 · The paper itself

Abstract

Purified PGL-1 and dPGL from M. leprae can prevent bacterial killing by intact phagocytes and cell-free antimicrobial systems. Both glycolipids completely abolished the antimicrobial effect of the acetaldehyde-XO-Fe2+ system. Because the cytotoxicity of this system is inhibited by catalase, SOD, mannitol, and ethanol, but not by heated SOD or catalase, these data suggest that toxicity is due to OH. generated by the Haber-Weiss reaction. That the antimicrobial killing in the XO system is completely blocked by the addition of PGL-1 or dPGL suggests that these glycolipids can act as OH. scavengers. A modest protective effect against the cytotoxicity of the MPO-H2O2-halide system by both PGL-1 and dPGL was also observed. The antimicrobial activity of the MPO system was abolished with chloride, but not iodide, as the halide. The effect of the M. leprae-derived glycolipid on bacterial killing by intact phagocytes was examined. Two linking antibodies were used to bind the dPGL to a rapidly growing test organism, S. aureus, a murine IgM mAb specific for the terminal glycoside of PGL-1, and a rabbit IgG anti-mouse IgM which bound the staphylococcal protein A via its Fc region. Examination by transmission EM of human monocyte-derived macrophages which had ingested staphylococci either coated with both antibodies and dPGL, or coated only with the IgG and IgM antibodies, demonstrated the presence of bacteria in phagosomes of control and IFN-gamma-activated macrophages. Activation of the macrophage monolayers by pretreatment with IFN-gamma markedly increased their staphylocidal activity. When dPGL coated staphylococci were ingested, killing by both control and IFN-gamma-activated macrophages was completely blocked. These results, suggesting that PGL-1 can scavenge reactive oxygen species and prevent microbial death within the phagosome, may in part explain the intracellular survival of M. leprae in certain cell types.

Indexed as

Antigens, BacterialAntioxidantsFree RadicalsGlycolipidsHumansInterferon-gammaMacrophage ActivationMacrophagesMycobacterium lepraeOxygenPeroxidaseXanthine OxidaseAntigens, BacterialAntioxidantsFree RadicalsGlycolipidsInterferon-gammaOxygenPeroxidasephenolic glycolipid I, Mycobacterium lepraeXanthine Oxidase

Identifiers

PMID2826638
PMCPMC2188820
OpenAlexW2133365276

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.