Evidence map›Paper›PMID 31041196›Full record

ArticleFrontiers in cellular and infection microbiology2019

Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.

Jennifer M Rudd, Sivasami Pulavendran, Harshini K Ashar, Jerry W Ritchey, Timothy A Snider, Jerry R Malayer, Montelongo Marie, Vincent T K Chow, Teluguakula Narasaraju

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular and infection microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 104 citations in OpenAlex.

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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

9 authors at 2 institutions in 2 countries.

Jennifer M RuddCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Sivasami PulavendranCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Harshini K AsharCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Jerry W RitcheyCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Timothy A SniderCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Jerry R MalayerCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Montelongo MarieCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Vincent T K ChowDepartment of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, National University Health System, Singapore, Singapore.
Teluguakula NarasarajuCenter for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK, United States.
Oklahoma State University · USNational University Health System · SG

Funding

ZFC3H1 Regulation of Host Defense and Influenza A Virus PathogenesisP20GM103648 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI CHENG, YONG · 2013 to 2022
$22.3M
NIGMS NIH HHS P20 GM103648
6 · The paper itself

Abstract

Exaggerated host innate immune responses have been implicated in severe influenza pneumonia. We have previously demonstrated that excessive neutrophils recruited during influenza infection drive pulmonary pathology through induction of neutrophil extracellular traps (NETs) and release of extracellular histones. Chemokine receptors (CRs) are essential in the recruitment and activation of leukocytes. Although neutrophils have been implicated in influenza pathogenesis, little is known about their phenotypic changes, including expression of CRs occurring in the infected -lung microenvironment. Here, we examined CC and CXC CRs detection in circulating as well as lung-recruited neutrophils during influenza infection in mice using flow cytometry analyses. Our studies revealed that lung-recruited neutrophils displayed induction of CRs, including CCR1, CCR2, CCR3, CCR5, CXCR1, CXCR3, and CXCR4, all of which were marginally induced in circulating neutrophils. CXCR2 was the most predominant CR observed in both circulating and lung-infiltrated neutrophils after infection. The stimulation of these induced CRs modulated neutrophil phagocytic activity, ligand-specific neutrophil migration, bacterial killing, and NETs induction

Indexed as

AnimalsDisease Models, AnimalFlow CytometryMiceNeutrophilsOrthomyxoviridaeOrthomyxoviridae InfectionsPneumonia, ViralReceptors, ChemokineReceptors, Chemokineacute lung injurychemokine receptorinfluenzamouse modelneutrophil

Identifiers

PMID31041196
PMCPMC6476945
OpenAlexW2939209922

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.