Evidence map›Paper›PMID 27555322›Full record

ArticleThe Journal of biological chemistry2016

Subversion of Schwann Cell Glucose Metabolism by Mycobacterium leprae.

Rychelle Clayde Affonso Medeiros, Karina do Carmo de Vasconcelos Girardi, Fernanda Karlla Luz Cardoso, Bruno de Siqueira Mietto, Thiago Gomes de Toledo Pinto, Lilian Sales Gomez, Luciana Silva Rodrigues, Mariana Gandini, Julio Jablonski Amaral, Sérgio Luiz Gomes Antunes and 10 more

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. The Role of Oxidative Stress in Peripheral Neuropathy.Journal of molecular neuroscience : MN · 2020
    Pooled it
  2. AMetabolites · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Genomic and Phenotypic Variations Among Thai-53 andPathogens (Basel, Switzerland) · 2024
    Article
  7. Adenosine AFrontiers in pharmacology · 2024
    Article
  8. Review
  9. What happens when Schwann cells are exposed toIBRO neuroscience reports · 2023
    Review
  10. Mitochondrial Dysfunction in Bacterial Infections.Pathogens (Basel, Switzerland) · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Gene Expression Profile ofFrontiers in medicine · 2022
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Essential Roles of PPARs in Lipid Metabolism during Mycobacterial Infection.International journal of molecular sciences · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 1 country.

Rychelle Clayde Affonso MedeirosFrom the Laboratório de Microbiologia Celular.
Karina do Carmo de Vasconcelos GirardiFrom the Laboratório de Microbiologia Celular.
Fernanda Karlla Luz CardosoFrom the Laboratório de Microbiologia Celular.
Bruno de Siqueira MiettoHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Thiago Gomes de Toledo PintoHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Lilian Sales Gomezthe Laboratório de Enzimologia e controle do metabolismo and.
Luciana Silva RodriguesImunopatologia, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro-RJ.
Mariana GandiniFrom the Laboratório de Microbiologia Celular.
Julio Jablonski Amaralthe National Institute of Metrology, Quality and Technology INMETRO, Rio de Janeiro-RJ.
Sérgio Luiz Gomes AntunesHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Suzana Corte-RealBiologia Estrutural, and.
Patricia Sammarco Rosathe Department of Biology, Lauro de Souza Lima Institute, Bauru-SP, and.
Maria Cristina Vidal PessolaniFrom the Laboratório de Microbiologia Celular.
José Augusto da Costa NeryHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Euzenir Nunes SarnoHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Leonardo Ribeiro Batista-SilvaHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Mauro Sola-Pennathe Laboratório de Enzimologia e controle do metabolismo and.
Marcus Fernandes Oliveirathe Laboratório de Bioquímica de Resposta ao Estresse, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Milton Ozório MoraesHanseníase, Oswaldo Cruz Institute, Fiocruz, Rio de Janeiro-RJ.
Flavio Alves LaraFrom the Laboratório de Microbiologia Celular, flavioalveslara2000@gmail.com.
Fundação Oswaldo Cruz · BRInstituto Lauro de Souza Lima · BRInstituto Nacional de Metrologia, Qualidade e Tecnologia · BRUniversidade do Estado do Rio de Janeiro · BRUniversidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium leprae, the intracellular etiological agent of leprosy, infects Schwann promoting irreversible physical disabilities and deformities. These cells are responsible for myelination and maintenance of axonal energy metabolism through export of metabolites, such as lactate and pyruvate. In the present work, we observed that infected Schwann cells increase glucose uptake with a concomitant increase in glucose-6-phosphate dehydrogenase (G6PDH) activity, the key enzyme of the oxidative pentose pathway. We also observed a mitochondria shutdown in infected cells and mitochondrial swelling in pure neural leprosy nerves. The classic Warburg effect described in macrophages infected by Mycobacterium avium was not observed in our model, which presented a drastic reduction in lactate generation and release by infected Schwann cells. This effect was followed by a decrease in lactate dehydrogenase isoform M (LDH-M) activity and an increase in cellular protection against hydrogen peroxide insult in a pentose phosphate pathway and GSH-dependent manner. M. leprae infection success was also dependent of the glutathione antioxidant system and its main reducing power source, the pentose pathway, as demonstrated by a 50 and 70% drop in intracellular viability after treatment with the GSH synthesis inhibitor buthionine sulfoximine, and aminonicotinamide (6-ANAM), an inhibitor of G6PDH 6-ANAM, respectively. We concluded that M. leprae could modulate host cell glucose metabolism to increase the cellular reducing power generation, facilitating glutathione regeneration and consequently free-radical control. The impact of this regulation in leprosy neuropathy is discussed.

Indexed as

Energy MetabolismCell LineGlucoseGlucosephosphate DehydrogenaseHumansLactic AcidLeprosy, TuberculoidMethionineMitochondriaMycobacterium lepraeSchwann CellsbuthionineGlucoseGlucosephosphate DehydrogenaseLactic AcidMethioninecell metabolismglucose-6-phosphate dehydrogenase (G6PD or G6PDH)glutathionehost-target therapyLeprosymitochondriamycobacterianeuronoxidative stresspentose phosphate pathway (PPP)

Identifiers

PMID27555322
PMCPMC5076808
OpenAlexW2517455432

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.