Evidence map›Paper›PMID 29621339›Full record

ArticlePLoS pathogens2018

Clarithromycin expands CD11b+Gr-1+ cells via the STAT3/Bv8 axis to ameliorate lethal endotoxic shock and post-influenza bacterial pneumonia.

Ho Namkoong, Makoto Ishii, Hideki Fujii, Kazuma Yagi, Takahiro Asami, Takanori Asakura, Shoji Suzuki, Ahmed E Hegab, Hirofumi Kamata, Sadatomo Tasaka and 8 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  10. Antibiotics as immunomodulators: a potential pharmacologic approach for ARDS treatment.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
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  19. Myeloid-Derived Suppressor Cells in Sepsis.Frontiers in immunology · 2019
    Review
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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

18 authors at 2 institutions in 1 country.

Ho NamkoongDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0001-6181-4284
Makoto IshiiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0003-4396-1664
Hideki FujiiDepartment of Immunology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
Kazuma YagiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Takahiro AsamiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-8574-5989
Takanori AsakuraDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0003-3122-6937
Shoji SuzukiDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Ahmed E HegabDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Hirofumi KamataDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0002-1807-5911
Sadatomo TasakaDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Koji AtarashiDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0001-5422-0736
Nobuhiro NakamotoDivision of Gastroenterology and Hepatology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Satoshi IwataCenter for Infectious Diseases and Infection Control, Keio University School of Medicine, Tokyo, Japan.
Kenya HondaDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.
Takanori KanaiDivision of Gastroenterology and Hepatology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Naoki HasegawaCenter for Infectious Diseases and Infection Control, Keio University School of Medicine, Tokyo, Japan.
Shigeo KoyasuDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.ORCID 0000-0001-9585-3038
Tomoko BetsuyakuDivision of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Keio University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrolides are used to treat various inflammatory diseases owing to their immunomodulatory properties; however, little is known about their precise mechanism of action. In this study, we investigated the functional significance of the expansion of myeloid-derived suppressor cell (MDSC)-like CD11b+Gr-1+ cells in response to the macrolide antibiotic clarithromycin (CAM) in mouse models of shock and post-influenza pneumococcal pneumonia as well as in humans. Intraperitoneal administration of CAM markedly expanded splenic and lung CD11b+Gr-1+ cell populations in naïve mice. Notably, CAM pretreatment enhanced survival in a mouse model of lipopolysaccharide (LPS)-induced shock. In addition, adoptive transfer of CAM-treated CD11b+Gr-1+ cells protected mice against LPS-induced lethality via increased IL-10 expression. CAM also improved survival in post-influenza, CAM-resistant pneumococcal pneumonia, with improved lung pathology as well as decreased interferon (IFN)-γ and increased IL-10 levels. Adoptive transfer of CAM-treated CD11b+Gr-1+ cells protected mice from post-influenza pneumococcal pneumonia. Further analysis revealed that the CAM-induced CD11b+Gr-1+ cell expansion was dependent on STAT3-mediated Bv8 production and may be facilitated by the presence of gut commensal microbiota. Lastly, an analysis of peripheral blood obtained from healthy volunteers following oral CAM administration showed a trend toward the expansion of human MDSC-like cells (Lineage-HLA-DR-CD11b+CD33+) with increased arginase 1 mRNA expression. Thus, CAM promoted the expansion of a unique population of immunosuppressive CD11b+Gr-1+ cells essential for the immunomodulatory properties of macrolides.

Indexed as

AnimalsAnti-Bacterial AgentsCD11b AntigenCell DifferentiationCell ProliferationClarithromycinGastrointestinal HormonesLipopolysaccharidesMaleMiceMice, Inbred C57BLMyeloid CellsNeuropeptidesOrthomyxoviridaeOrthomyxoviridae InfectionsPhagocytosisAnti-Bacterial AgentsCD11b AntigenClarithromycinGastrointestinal HormonesLipopolysaccharidesNeuropeptidesProk2 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID29621339
PMCPMC5886688
OpenAlexW2796143894

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.