Evidence map›Paper›PMID 42056243›Full record

ArticleCommunications biology2026

Macrophage-derived MBL restrains coronavirus-induced pulmonary inflammation by modulating metabolic regulator PKM2-mediated NLRP3 activation.

Yan Liu, Jinjin Guo, Yueyang Lu, Weijie Shao, Bo Chang, Jialiang Luo, Zhuojun Zheng, Xiao Lu, Lin Yu, Ke Ma and 3 more

Abstract read
In one paragraph

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

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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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Yan Liu *Institute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Jinjin Guo *Institute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Yueyang Lu *Institute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Weijie ShaoDepartment of Immunology, Guangdong Province Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Bo ChangDepartment of Immunology, Guangdong Province Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Jialiang LuoInstitute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Zhuojun ZhengInstitute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China.
Xiao LuDepartment of Immunology, Guangdong Province Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Lin YuThe Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Ke MaZhongshan People's Hospital, Zhongshan, Guangdong, China.
Mingyong WangXinxiang Key Laboratory of Immunoregulation and Molecular Diagnostics, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan, China. wmy118@126.com.ORCID http://orcid.org/0000-0003-1057-2603
Daming ZuoInstitute of Molecular Immunology, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, China. zdaming@smu.edu.cn.ORCID http://orcid.org/0000-0003-2003-9474
Jia ZhouDepartment of Immunology, Guangdong Province Key Laboratory of Proteomics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China. yuguomm@smu.edu.cn.ORCID http://orcid.org/0000-0001-6107-5469

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The precise mechanisms governing innate immune response to coronaviruses remain elusive. Our study reveals that mannose-binding lectin (MBL), a key pattern recognition molecule, exhibits significant upregulation in PBMCs from COVID-19 patients, with expression levels positively correlating with clinical severity. Through intranasal coronavirus MHV-A59 challenge in MBL-deficient mice, we demonstrate that macrophage-derived MBL attenuates viral pneumonia by limiting NLRP3 inflammasome hyperactivation. Mechanistically, MBL directly binds pyruvate kinase M2 (PKM2), an interaction significantly enhanced upon viral stimulation. Crucially, MBL competitively inhibits O-GlcNAcylation at PKM2 Thr405/Ser406 residues, thereby disrupting PKM2 tetramer-to-dimer transition and its subsequent nuclear translocation. The MBL-mediated metabolic reprogramming effectively dampens NLRP3 inflammasome activation, with wild-type mice exhibiting markedly reduced caspase-1 cleavage and IL-1β maturation relative to MBL-deficient mice following MHV-A59 infection. Genetic ablation of NLRP3 abolished the differential susceptibility between wild-type and MBL-deficient animals, confirming NLRP3 as the critical downstream effector. Pharmacological inhibition of either PKM2 or NLRP3 restored cytokine homeostasis in virus-infected MBL-deficient mice. These findings establish a previously unrecognized regulatory pathway in which macrophage-specific MBL fine-tunes antiviral immunity through the PKM2-NLRP3 axis. Our work provides crucial insights into the sophisticated interplay between innate immunity and cellular metabolism, laying the groundwork for developing host-directed therapies against coronaviruses.

Indexed as

Carrier ProteinsCOVID-19MacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinPyruvate KinaseAnimalsHumansImmunity, InnateInflammasomesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutSARS-CoV-2Thyroid Hormone-Binding ProteinsCarrier ProteinsInflammasomesMembrane ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePkm protein, mousePyruvate KinaseThyroid Hormone-Binding Proteins

Identifiers

PMID42056243
PMCPMC13333995

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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.