Evidence map›Paper›PMID 11254592›Full record

ArticleInfection and immunity2001

Interleukin-10 stimulates Coxiella burnetii replication in human monocytes through tumor necrosis factor down-modulation: role in microbicidal defect of Q fever.

E Ghigo, C Capo, D Raoult, J L Mege

Abstract read
In one paragraph

Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 89 citations in OpenAlex.

  1. Review
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  5. Identification and Characterization of an HtrA Sheddase Produced byInternational journal of molecular sciences · 2023
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  8. Infection and Persistence ofInternational journal of molecular sciences · 2023
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  15. Article
  16. Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021
    Review
  17. Early Cytokine Response After Vaccination withJournal of veterinary research · 2018
    Article
  18. Coxiella burnetii Lipopolysaccharide: What Do We Know?International journal of molecular sciences · 2017
    Review
  19. Review
  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

4 authors at 1 institution in 1 country.

E GhigoUnité des Rickettsies, CNRS UMR 6020, Université de la Méditerranée, Marseille, France.
C Capo
D Raoult
J L Mege
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic form of the disease is associated with the overproduction of interleukin-10 and deficient C. burnetii killing by monocytes. We hypothesized that the replication of C. burnetii inside monocytes requires a macrophage-deactivating cytokine such as interleukin-10. In the absence of interleukin-10, C. burnetii survived but did not replicate in monocytes. C. burnetii replication (measured 15 days) was induced in interleukin-10-treated monocytes. This effect of interleukin-10 is specific since transforming growth factor beta1 had no effect on bacterial replication. C. burnetii replication involves the down-modulation of tumor necrosis factor (TNF) release. First, interleukin-10 suppressed C. burnetii-stimulated production of TNF. Second, the addition of recombinant TNF to interleukin-10-treated monocytes inhibited bacterial replication. Third, the incubation of infected monocytes with neutralizing anti-TNF antibodies favored C. burnetii replication. On the other hand, deficient C. burnetii killing by monocytes from patients with chronic Q fever involves interleukin-10. Indeed, C. burnetii replication was observed in monocytes from patients with Q fever endocarditis, but not in those from patients with acute Q fever. Bacterial replication was inhibited by neutralizing anti-interleukin-10 antibodies. As monocytes from patients with endocarditis overproduced interleukin-10, the defective bacterial killing is likely related to endogenous interleukin-10. These results suggest that interleukin-10 enables monocytes to support C. burnetii replication and to favor the development of chronic Q fever.

Indexed as

Blood Bactericidal ActivityAntigens, CDCoxiella burnetiiDown-RegulationEndocarditis, BacterialHumansInterleukin-10MonocytesQ FeverReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IITransforming Growth Factor betaTumor Necrosis Factor-alphaAntigens, CDInterleukin-10Receptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IITransforming Growth Factor betaTumor Necrosis Factor-alpha

Identifiers

PMID11254592
PMCPMC98164
OpenAlexW2096560542

What OpenQuestion holds

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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.