Evidence map›Paper›PMID 24987031›Full record

ArticleThe Journal of infectious diseases2014

Platelets direct monocyte differentiation into epithelioid-like multinucleated giant foam cells with suppressive capacity upon mycobacterial stimulation.

Yonghong Feng, Anca Dorhoi, Hans-Joachim Mollenkopf, Hongyun Yin, Zhengwei Dong, Ling Mao, Jun Zhou, Aixiao Bi, Stephan Weber, Jeroen Maertzdorf and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

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  7. Platelets promote human macrophages-mediated macropinocytosis ofFrontiers in cellular and infection microbiology · 2023
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  18. Platelets Regulate Pulmonary Inflammation and Tissue Destruction in Tuberculosis.American journal of respiratory and critical care medicine · 2018
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  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Yonghong FengDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany Shanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University, China.
Anca DorhoiDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hans-Joachim MollenkopfMax Planck Institute for Infection Biology, Core Facility Microarray/Genomics, Berlin, Germany.
Hongyun YinShanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University, China.
Zhengwei DongDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University.
Ling MaoShanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University, China.
Jun ZhouDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University.
Aixiao BiShanghai Key Lab of Tuberculosis, Shanghai Pulmonary Hospital, Tongji University, China.
Stephan WeberDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Jeroen MaertzdorfDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Gang ChenDepartment of Pathology, Shanghai Pulmonary Hospital, Tongji University.
Yang ChenBioinformatics Division and Center for Synthetic and Systems Biology, TNLIST, Department of Automation, Tsinghua University, Beijing, China.
Stefan H E KaufmannDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Max Planck Institute for Infection Biology · DEShanghai Pulmonary Hospital · CNTongji University · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelioid, foam, and multinucleated giant cells (MNGCs) are characteristics of tuberculosis granulomas, yet the precise genesis and functions of these transformed macrophages are unclear. We evaluated the role of platelets as drivers of macrophage transformation in mycobacterial infection.

methodsWe employed flow cytometry and microscopy to assess cellular phenotype and phagocytosis. Immune assays allowed quantification of cytokines and chemokines, whereas gene microarray technology was applied to estimate global transcriptome alterations. Immunohistochemical investigations of tuberculosis granulomas substantiated our findings at the site of infection.

resultsMonocytes differentiated in presence of platelets (MP-Macs) acquired a foamy, epithelioid appearance and gave rise to MNGCs (MP-MNGCs). MP-Macs up-regulated activation markers, phagocytosed mycobacteria, and released abundant interleukin 10. Upon extended culture, MP-Macs shared transcriptional features with epithelioid cells and M2 macrophages and up-regulated CXCL5 transcripts. In line with this, CXCL5 concentrations were significantly increased in airways of active tuberculosis patients. The platelet-specific CD42b antigen was detected in MP-Macs, likewise in macrophages, MNGCs, and epithelioid cells within tuberculosis granulomas, along with the platelet aggregation-inducing factor PDPN.

conclusionsPlatelets drive macrophage differentiation into MNGCs with characteristics of epithelioid, foam, and giant cells observed in tuberculosis granulomas. Our data define platelets as novel participants in tuberculosis pathogenesis.

Indexed as

ImmunomodulationAdultBiomarkersBlood PlateletsCoculture TechniquesFemaleFoam CellsGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksGranulomaHumansInterleukin-10LipopolysaccharidesMaleMiddle AgedBiomarkersInterleukin-10LipopolysaccharidesCXCL5macrophagemultinucleated giant cellplatelettuberculosis

Identifiers

PMID24987031
PMCPMC4224136
OpenAlexW2133786872

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.