Evidence map›Paper›PMID 38295799›Full record

ArticleImmunity2024

A GPCR-neuropeptide axis dampens hyperactive neutrophils by promoting an alternative-like polarization during bacterial infection.

Naina Gour, Hwan Mee Yong, Aishwarya Magesh, Aishwarya Atakkatan, Felipe Andrade, Stephane Lajoie, Xinzhong Dong

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  4. An Itch Receptor Drives Melanoma.bioRxiv : the preprint server for biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Naina GourSolomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Hwan Mee YongDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Aishwarya MageshKrieger School of Arts and Sciences, Johns Hopkins University, Baltimore, MD, USA; Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Aishwarya AtakkatanSolomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, MD, USA; Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Felipe AndradeDivision of Rheumatology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Stephane LajoieDepartment of Otolaryngology, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Xinzhong DongSolomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, Baltimore, MD, USA; Howard Hughes Medical Institute, Chevy Chase, MD, USA. Electronic address: xdong2@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

Functional Analysis of Mrgpr Family in itch sensationR37NS054791 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Xinzhong Dong · 2022 to 2026
$2.9M
Neuronally-driven accumulation of glycolytic MafB+MHCIIhi IMs drive airway allergyR01AI170709 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Stephane Lajoie · 2023 to 2026
$2.5M
Dysregulated sensing of invertebrate tropomyosin through dectin-1 confers susceptibility to type-2-mediated allergic diseasesR01AI127644 · NIAID · JOHNS HOPKINS UNIVERSITY · PI LAJOIE, STEPHANE · 2017 to 2021
$2.0M
The role of complement citrullination in RA pathogenesisR01AR069569 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2016 to 2020
$1.8M
Autoimmunity to LINE-1-encoded antigens in SLE pathogenesisR21AI147598 · NIAID · JOHNS HOPKINS UNIVERSITY · PI ANDRADE, FELIPE · 2020 to 2021
$450k
Howard Hughes Medical InstituteNIAID NIH HHS R01 AI127644NIAID NIH HHS R01 AI170709NIAID NIH HHS R21 AI147598NIAMS NIH HHS R01 AR069569NINDS NIH HHS R37 NS054791
6 · The paper itself

Abstract

The notion that neutrophils exist as a homogeneous population is being replaced with the knowledge that neutrophils adopt different functional states. Neutrophils can have a pro-inflammatory phenotype or an anti-inflammatory state, but how these states are regulated remains unclear. Here, we demonstrated that the neutrophil-expressed G-protein-coupled receptor (GPCR) Mrgpra1 is a negative regulator of neutrophil bactericidal functions. Mrgpra1-mediated signaling was driven by its ligand, neuropeptide FF (NPFF), which dictated the balance between pro- and anti-inflammatory programming. Specifically, the Mrgpra1-NPFF axis counter-regulated interferon (IFN) γ-mediated neutrophil polarization during acute lung infection by favoring an alternative-like polarization, suggesting that it may act to balance overzealous neutrophilic responses. Distinct, cross-regulated populations of neutrophils were the primary source of NPFF and IFNγ during infection. As a subset of neutrophils at steady state expressed NPFF, these findings could have broad implications in various infectious and inflammatory diseases. Therefore, a neutrophil-intrinsic pathway determines their cellular fate, function, and magnitude of infection.

Indexed as

Bacterial InfectionsNeuropeptidesAnti-Inflammatory AgentsHumansNeutrophilsReceptors, G-Protein-CoupledReceptors, NeuropeptideAnti-Inflammatory AgentsNeuropeptidesReceptors, G-Protein-CoupledReceptors, NeuropeptideIFNγlung infectionMrgpra1 GPCRneuropeptide FFneutrophil polarizationneutrophilsNPFF

Identifiers

PMID38295799
PMCPMC10940224
OpenAlexW4391375855

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.