Evidence map›Paper›PMID 8406806›Full record

ArticleInfection and immunity1993

Regulation of murine macrophage effector functions by lipoarabinomannan from mycobacterial strains with different degrees of virulence.

L B Adams, Y Fukutomi, J L Krahenbuhl

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  15. The continuing challenges of leprosy.Clinical microbiology reviews · 2006
    Review
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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 B AdamsG. W. Long Hansen's Disease Center, Louisiana State University, Baton Rouge 70894.
Y Fukutomi
J L Krahenbuhl
National Hansen's Disease Program · US

Funding

IMMUNOLOGY AND IMMUNOTHERAPY OF LEPROSYR01AI022442 · NIAID · NATIONAL HANSEN'S DISEASE PROGRAM · PI KRAHENBUHL, JAMES L · 1989 to 1990
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IMMUNOLOGY &IMMUNOTHERAPY OF LEPROSYR22AI022442 · NIAID · NATIONAL HANSEN'S DISEASE PROGRAM · PI KRAHENBUHL, JAMES L · 1985 to 1990
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NIAID NIH HHS NIAID AI22442
6 · The paper itself

Abstract

Lipoarabinomannan (LAM) is the major arabinose- and mannose-containing phosphorylated lipopolysaccharide (LPS) in mycobacterial cell walls. LAM preparations from a virulent strain (Erdman) (LAM(Erdman)) and an attenuated strain (H37Ra) (LAMH37Ra) of Mycobacterium tuberculosis, as well as from M. leprae (a virulent mycobacterium), were analyzed for their effects on various macrophage (M phi) effector functions. LAMH37Ra, like gram-negative LPS, exhibited a dose-dependent ability to induce tumor necrosis factor alpha (TNF-alpha) production in normal M phi, and gamma interferon (IFN-gamma) priming of the M phi greatly augmented the levels of TNF-alpha. However, the effects of LAMH37Ra were unaffected by polymyxin B, which totally abrogated the effects of LPS. LAM(Erdman) and LAM from M. leprae, on the other hand, induced virtually no TNF-alpha production. Analysis of M phi mRNA by reverse transcription-polymerase chain reaction revealed that the levels of production. Analysis of M phi mRNA by reverse transcription-polymerase chain reaction revealed that the levels of TNF-alpha mRNA induced by the various preparations correlated with the levels of TNF-alpha protein detected. Interestingly, both LAMH37Ra and LAM(Erdman) could block subsequent IFN-gamma- and LPS-induced M phi activation, a previously reported measure of the potent ability of LAM to down-regulate M phi effector functions. Two lines of evidence suggested, however, that M phi cyclooxygenase products did not play a role in this down-regulation. LAMH37Ra and LPS could induce the production of NO2- in both normal and IFN-gamma-primed M phi, whereas LAM(Erdman) could stimulate NO2- production only in primed M phi. Both LAMH37Ra and LAM(Erdman) could substitute for LPS as a triggering signal for IFN-gamma-primed M phi in a toxoplasma killing assay. The triggering ability of LAM(Erdman), however, was abrogated by an anti-TNF-alpha antibody, suggesting that sufficient TNF-alpha production was stimulated by LAM(Erdman) to drive a M phi function relevant in host resistance. Thus, mycobacterial LAM is a potent regulator of M phi functions, a fact that may have important consequences in mycobacterial disease.

Indexed as

AnimalsBlood Bactericidal ActivityDinoprostoneGene ExpressionIndomethacinInterferon-gammaLipopolysaccharidesMacrophage ActivationMacrophagesMiceMycobacteriumNitritesProstaglandin-Endoperoxide SynthasesRNA, MessengerTumor Necrosis Factor-alphaDinoprostoneIndomethacinInterferon-gammalipoarabinomannanLipopolysaccharidesNitritesProstaglandin-Endoperoxide SynthasesRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID8406806
PMCPMC281141
OpenAlexW1893103753

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.