Evidence map›Paper›PMID 34608123›Full record

ArticleCell discovery2021

Interception of host fatty acid metabolism by mycobacteria under hypoxia to suppress anti-TB immunity.

Hua Yang, Fei Wang, Xinya Guo, Feng Liu, Zhonghua Liu, Xiangyang Wu, Mengmeng Zhao, Mingtong Ma, Haipeng Liu, Lianhua Qin and 18 more

Open access · goldAbstract read
In one paragraph

Article in Cell discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-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

20 citing papers in PubMed, 34 citations in OpenAlex.

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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

28 authors at 5 institutions in 2 countries.

Hua Yang *Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Fei Wang *Department of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Xinya Guo *Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Feng Liu *Shanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Zhonghua LiuShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Xiangyang WuDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Mengmeng ZhaoDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Mingtong MaDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Haipeng LiuShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Lianhua QinShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Lin WangShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Tianqi TangDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Wei ShaTuberculosis Center for Diagnosis and Treatment, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Yang WangDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Jianxia ChenShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Xiaochen HuangShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Jie WangShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Cheng PengDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Ruijuan ZhengShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Fen TangDepartment of Microbiology and Immunology, Tongji University School of Medicine, Shanghai, China.
Lu ZhangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, China.
Chunyan WuDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Stefan H OehlersTuberculosis Research Program at the Centenary Institute, The University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0003-0260-672X
Zhigang SongEastern China Center for Pathogen Discovery and Research, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Jialei SheEastern China Center for Pathogen Discovery and Research, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Hua FengOmics Core of Bio-Med Big Data Center, CAS-MPG Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Xunwei XieChina Zebrafish Resource Center, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei, China.
Baoxue GeShanghai Key Laboratory of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China. gebaoxue@sibs.ac.cn.ORCID http://orcid.org/0000-0002-4086-8299
Tongji University · CNChinese Academy of Sciences · CNShanghai Public Health Clinical Center · CNFudan University · CNThe University of Sydney · AU

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32030038National Natural Science Foundation of China (National Science Foundation of China) 81870002
6 · The paper itself

Abstract

Pathogenic mycobacteria induce the formation of hypoxic granulomas during latent tuberculosis (TB) infection, in which the immune system contains, but fails to eliminate the mycobacteria. Fatty acid metabolism-related genes are relatively overrepresented in the mycobacterial genome and mycobacteria favor host-derived fatty acids as nutrient sources. However, whether and how mycobacteria modulate host fatty acid metabolism to drive granuloma progression remains unknown. Here, we report that mycobacteria under hypoxia markedly secrete the protein Rv0859/MMAR_4677 (Fatty-acid degradation A, FadA), which is also enriched in tuberculous granulomas. FadA acts as an acetyltransferase that converts host acetyl-CoA to acetoacetyl-CoA. The reduced acetyl-CoA level suppresses H3K9Ac-mediated expression of the host proinflammatory cytokine Il6, thus promoting granuloma progression. Moreover, supplementation of acetate increases the level of acetyl-CoA and inhibits the formation of granulomas. Our findings suggest an unexpected mechanism of a hypoxia-induced mycobacterial protein suppressing host immunity via modulation of host fatty acid metabolism and raise the possibility of a novel therapeutic strategy for TB infection.

Identifiers

PMID34608123
PMCPMC8490369
OpenAlexW3203725040

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.