Evidence map›Paper›PMID 42071231›Full record

ArticleRespiratory research2026

IL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1ɑ/glycolysis pathway.

Yuchi Gao, Longbin Cao, Xiuhua Huang, Guikai Duan, Bingying Lin, Junai Zhang, Wenyi Liu, Chen Chen, Junxiang Li, Mi Liu and 6 more

Abstract read
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In one paragraph

Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

16 authors.

Yuchi Gao *Department of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Longbin Cao *Department of Clinical Laboratory, The Seventh Affiliated Hospital, Southern Medical University, Foshan, Guangdong Province, 528244, China.
Xiuhua HuangDepartment of Pathology, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, 518105, China.
Guikai DuanDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Bingying LinDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Junai ZhangGuangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, School of Medical Technology, The First Dongguan Affiliated Hospital, Guangdong Medical University, Dongguan, 523808, China.
Wenyi LiuDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China.
Chen ChenDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China.
Junxiang LiDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Mi LiuDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Xiang LiDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Hao ChenDepartment of Clinical Laboratory, Shenzhen Maternity and Child Healthcare Hospital, Women and Children's Medical Center, Southern Medical University, Shenzhen, Guangdong Province, 518028, China.
Rong LiuDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China.
Juan TangDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China.
Jing XiaoDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China.
Yuanbin LuDepartment of Clinical Laboratory, Shenzhen Bao'an District Songgang People's Hospital, Shenzhen, Guangdong Province, 518105, China. 451001402@qq.com.

Funding

GuangDong Basic and Applied Basic Research Foundation 2019A1515110066Medical Science and Technology Research Foundation of Guangdong A2023068Science and Technology Program of Shenzhen JCYJ20220530144402005Shenzhen Futian District Health Public Welfare Research Project FTW2021057
6 · The paper itself

Abstract

backgroundIL-36γ coordinates macrophage activation and is essential for defense against Mycobacterium tuberculosis (Mtb), but the mechanisms remains poorly understood. Aerobic glycolysis plays a critical role in macrophages intrinsic control of Mtb infection. This study aimed to investigate the potential effects of IL-36γ on macrophages energy metabolism transformation from mitochondrial oxidative phosphorylation to aerobic glycolysis in response to Mtb infection.

methodsThe expression of IL-36γ in lung tissues, PBMCs and serum was analyzed using Immunohistochemistry, ELISA and RT-qPCR, while the role and mechanism of IL-36γ on macrophages energy metabolism transformation duing Mtb infection were investigated by RT-qPCR, ELISA, Western blot and colony-forming unit assay.

resultsWe demonstrated IL-36γ enhanced the aerobic glycolysis, and downregulated the mitochondrial oxidative phosphorylation in Mtb infected macrophages. Furthermore, IL-36γ upregulated the expression of HIF-1α and IFN-γ in macrophages through the NF-κB/ERK/JNK signaling pathway, especially in macrophages infected with Mtb, where it induced the expression of large amounts of HIF-1α and IFN-γ. Moreover, IL-36γ promoted aerobic glycolysis through inducing the expression of HIF-1α in macrophages during Mtb infection. Meanwhile, HIF-1α was required for IL-36γ-mediated control of Mtb infection. Interestingly, the expression of IL-36γ was increased in lung tissues, PBMCs and serum from patients with active pulmonary tuberculosis and correlated with monocytes/macrophages immune response and IFN-γ levels, displayed an appreciable diagnostic value.

conclusionIL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1α/ glycolysis pathway. IL-36γ may be a potential treatment target and useful biomarker for tuberculosis.

Indexed as

Interleukin-1MacrophagesMycobacterium tuberculosisTuberculosis, PulmonaryAdolescentAdultAgedBiomarkersCase-Control StudiesGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitInterferon-gammaLungMiddle AgedMitochondriaBiomarkersHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitIL36G protein, humanInterferon-gammaInterleukin-1Aerobic glycolysisBiomarkerHIF-1αIFN-γIL-36γTuberculosis

Identifiers

PMID42071231
PMCPMC13317291

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.