Evidence map›Paper›PMID 31709673›Full record

ArticleCellular microbiology2020

A1 adenosine receptor signaling reduces Streptococcus pneumoniae adherence to pulmonary epithelial cells by targeting expression of platelet-activating factor receptor.

Manmeet Bhalla, Jun Hui Yeoh, Claire Lamneck, Sydney E Herring, Essi Y I Tchalla, Lauren R Heinzinger, John M Leong, Elsa N Bou Ghanem

Open access · greenAbstract read
In one paragraph

Article in Cellular microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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  11. Anti-Inflammatory Metabolites in the Pathogenesis of Bacterial Infection.Frontiers in cellular and infection microbiology · 2022
    Review
  12. Article
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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

8 authors at 2 institutions in 1 country.

Manmeet BhallaDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.
Jun Hui YeohDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.
Claire LamneckDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts.
Sydney E HerringDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.
Essi Y I TchallaDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.
Lauren R HeinzingerDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.
John M LeongDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts.
Elsa N Bou GhanemDepartment of Microbiology and Immunology, State University of New York at Buffalo School of Medicine, Buffalo, New York.ORCID 0000-0002-8936-1341
University at Buffalo, State University of New York · USTufts University · US

Funding

The role of extracellular adenosine in age-driven susceptibility to S. pneumoniae lung infectionR00AG051784 · NIA · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI BOU GHANEM, ELSA · 2018 to 2020
$719k
NIA NIH HHS R00 AG051784
6 · The paper itself

Abstract

Extracellular adenosine production is crucial for host resistance against Streptococcus pneumoniae (pneumococcus) and is thought to affect antibacterial immune responses by neutrophils. However, whether extracellular adenosine alters direct host-pathogen interaction remains unexplored. An important determinant for lung infection by S. pneumoniae is its ability to adhere to the pulmonary epithelium. Here we explored whether extracellular adenosine can directly impact bacterial adherence to lung epithelial cells. We found that signaling via A1 adenosine receptor significantly reduced the ability of pneumococci to bind human pulmonary epithelial cells. A1 receptor signaling blocked bacterial binding by reducing the expression of platelet-activating factor receptor, a host protein used by S. pneumoniae to adhere to host cells. In vivo, A1 was required for control of pneumococcal pneumonia as inhibiting it resulted in increased host susceptibility. As S. pneumoniae remain a leading cause of community-acquired pneumonia in the elderly, we explored the role of A1 in the age-driven susceptibility to infection. We found no difference in A1 pulmonary expression in young versus old mice. Strikingly, triggering A1 signaling boosted host resistance of old mice to S. pneumoniae pulmonary infection. This study demonstrates a novel mechanism by which extracellular adenosine modulates resistance to lung infection by targeting bacterial-host interactions.

Indexed as

Pneumonia, PneumococcalStreptococcus pneumoniaeAge FactorsAnimalsBacterial AdhesionCell LineEpithelial CellsHost-Pathogen InteractionsHumansLungMiceMice, Inbred C57BLPlatelet Membrane GlycoproteinsReceptor, Adenosine A1Receptors, G-Protein-Coupledplatelet activating factor receptorPlatelet Membrane GlycoproteinsReceptor, Adenosine A1Receptors, G-Protein-Coupledagingbacterial bindingextracellular adenosinemicrobial-cell interactionstreptococci

Identifiers

PMID31709673
PMCPMC6980675
OpenAlexW2988197128

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.