Evidence map›Paper›PMID 37338372›Full record

ArticleInfection and immunity2023

Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague.

Hayley M Theriot, Priyangi A Malaviarachchi, Madeleine G Scott, Kenneth T Appell, Srijon K Banerjee, Roger D Pechous

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Infection and immunity, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Morphopathology of the lesions induced by SARS-CoV-2 infection in the lungs.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    Article
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

6 authors at 2 institutions in 1 country.

Hayley M TheriotDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Priyangi A MalaviarachchiDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Madeleine G ScottDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Kenneth T AppellDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.
Srijon K BanerjeeDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
Roger D PechousDepartment of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.ORCID 0000-0002-5434-4744
University of Arkansas for Medical Sciences · USUniversity of Pittsburgh · US

Funding

Defining the Role of the Plasminogen Activator Protease in the Early Events that Establish Primary Pneumonic PlagueR01AI153252 · NIAID · UNIV OF ARKANSAS FOR MED SCIS · PI HUANG, LU, PECHOUS, ROGER D · 2021 to 2025
$1.7M
NIAID NIH HHS R01 AI153252
6 · The paper itself

Abstract

Inhalation of respiratory droplets infected with Yersinia pestis results in a rapidly progressing and lethal necrotic pneumonia called primary pneumonic plague. Disease manifests as biphasic, with an initial preinflammatory phase with rapid bacterial replication in the lungs absent readily detectable host immune responses. This is followed by the onset of a proinflammatory phase that sees the dramatic upregulation of proinflammatory cytokines and extensive neutrophil accumulation in the lungs. The plasminogen activator protease (Pla) is an essential virulence factor that is responsible for survival of Y. pestis in the lungs. Our lab recently showed that Pla functions as an adhesin that promotes binding to alveolar macrophages to facilitate translocation of effector proteins called Yops into the cytosol of target host cells via a type 3 secretion system (T3SS). Loss of Pla-mediated adherence disrupted the preinflammatory phase of disease and resulted in early neutrophil migration to the lungs. While it is established that

Indexed as

PlagueYersinia pestisAnimalsDisease Models, AnimalInterleukin-17LungMiceMice, Inbred C57BLNeutrophil InfiltrationInterleukin-17IL-17plaguepneumonic plagueYersiniaYersinia pestis

Identifiers

PMID37338372
PMCPMC10353359
OpenAlexW4381308597

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.