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Record W3010008632 · doi:10.1073/pnas.1919211117

Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis

2020· article· en· W3010008632 on OpenAlexafffund
Md. Aejazur Rahman, Bridgette M. Cumming, Kelvin W. Addicott, Hayden T. Pacl, Shannon Russell, Kievershen Nargan, Threnesan Naidoo, Pratistadevi K. Ramdial, John Adamson, Rui Wang, Adrie J. C. Steyn

Bibliographic record

VenueProceedings of the National Academy of Sciences · 2020
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicSulfur Compounds in Biology
Canadian institutionsYork University
FundersNational Institute of Allergy and Infectious DiseasesMedical Research CouncilGovernment of CanadaCenter for AIDS Research, University of Alabama at BirminghamSouth African Medical Research CouncilNational Research FoundationNational Institutes of HealthUniversity of Alabama at BirminghamCenter for AIDS Research, University of WashingtonUniversity of AlabamaNatural Sciences and Engineering Research Council of CanadaCRDF GlobalNational Institute of Diabetes and Digestive and Kidney DiseasesBill and Melinda Gates Foundation
KeywordsImmune systemGlycolysisInnate immune systemMycobacterium tuberculosisEffectorPentose phosphate pathwayTuberculosisPathogenesisBiologyImmunologyMicrobiologyMedicineMetabolismBiochemistryPathology

Abstract

fetched live from OpenAlex

The ubiquitous gasotransmitter hydrogen sulfide (H 2 S) has been recognized to play a crucial role in human health. Using cystathionine γ-lyase (CSE)-deficient mice, we demonstrate an unexpected role of H 2 S in Mycobacterium tuberculosis ( Mtb ) pathogenesis. We showed that Mtb- infected CSE −/− mice survive longer than WT mice, and support reduced pathology and lower bacterial burdens in the lung, spleen, and liver. Similarly, in vitro Mtb infection of macrophages resulted in reduced colony forming units in CSE −/− cells. Chemical complementation of infected WT and CSE −/− macrophages using the slow H 2 S releaser GYY3147 and the CSE inhibitor DL-propargylglycine demonstrated that H 2 S is the effector molecule regulating Mtb survival in macrophages. Furthermore, we demonstrate that CSE promotes an excessive innate immune response, suppresses the adaptive immune response, and reduces circulating IL-1β, IL-6, TNF-α, and IFN-γ levels in response to Mtb infection. Notably, Mtb infected CSE −/− macrophages show increased flux through glycolysis and the pentose phosphate pathway, thereby establishing a critical link between H 2 S and central metabolism. Our data suggest that excessive H 2 S produced by the infected WT mice reduce HIF-1α levels, thereby suppressing glycolysis and production of IL-1β, IL-6, and IL-12, and increasing bacterial burden. Clinical relevance was demonstrated by the spatial distribution of H 2 S-producing enzymes in human necrotic, nonnecrotic, and cavitary pulmonary tuberculosis (TB) lesions. In summary, CSE exacerbates TB pathogenesis by altering immunometabolism in mice and inhibiting CSE or modulating glycolysis are potential targets for host-directed TB control.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.004

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.019
GPT teacher head0.272
Teacher spread0.253 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations93
Published2020
Admission routes2
Has abstractyes

Explore more

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