Evidence map›Paper›PMID 35072520›Full record

ArticleInfection and immunity2022

Neutrophil-Associated Responses to Vibrio cholerae Infection in a Natural Host Model.

Dustin Farr, Dhrubajyoti Nag, Walter J Chazin, Simone Harrison, Ryan Thummel, Xixia Luo, Saumya Raychaudhuri, Jeffrey H Withey

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 2 countries.

Dustin FarrDepartment of Biochemistry, Microbiology, and Immunology, Wayne State Universitygrid.254444.7 School of Medicine, Detroit, Michigan, USA.
Dhrubajyoti NagDepartment of Biochemistry, Microbiology, and Immunology, Wayne State Universitygrid.254444.7 School of Medicine, Detroit, Michigan, USA.
Walter J ChazinDepartment of Biochemistry, Center for Structural Biology, Vanderbilt Universitygrid.152326.1, Nashville, Tennessee, USA.
Simone HarrisonDepartment of Biochemistry, Center for Structural Biology, Vanderbilt Universitygrid.152326.1, Nashville, Tennessee, USA.
Ryan ThummelDepartment of Ophthalmology, Visual and Anatomical Sciences, Wayne State Universitygrid.254444.7 School of Medicine, Detroit, Michigan, USA.
Xixia LuoDepartment of Ophthalmology, Visual and Anatomical Sciences, Wayne State Universitygrid.254444.7 School of Medicine, Detroit, Michigan, USA.
Saumya RaychaudhuriCSIR-Institute of Microbial Technology, Chandigarh, India.
Jeffrey H WitheyDepartment of Biochemistry, Microbiology, and Immunology, Wayne State Universitygrid.254444.7 School of Medicine, Detroit, Michigan, USA.ORCID 0000-0001-6856-5604
Wayne State University · USVanderbilt University · USInstitute of Microbial Technology · IN

Funding

Mechanisms for Vibrio cholerae colonization and pathogenesis in zebrafishR01AI127390 · NIAID · WAYNE STATE UNIVERSITY · PI WITHEY, JEFFREY H · 2017 to 2021
$1.9M
NIAID NIH HHS R01 AI127390
6 · The paper itself

Abstract

Vibrio cholerae, the cause of human cholera, is an aquatic bacterium found in association with a variety of animals in the environment, including many teleost fish species. V. cholerae infection induces a proinflammatory response followed by a noninflammatory convalescent phase. Neutrophils are integral to this early immune response. However, the relationship between the neutrophil-associated protein calprotectin and V. cholerae has not been investigated, nor have the effects of limiting transition metals on V. cholerae growth. Zebrafish are useful as a natural V. cholerae model as the entire infectious cycle can be recapitulated in the presence of an intact intestinal microbiome and mature immune responses. Here, we demonstrate that zebrafish produce a significant neutrophil, interleukin 8 (IL-8), and calprotectin response following V. cholerae infection. Bacterial growth was completely inhibited by purified calprotectin protein or the chemical chelator

Indexed as

CholeraVibrio choleraeAnimalsLeukocyte L1 Antigen ComplexNeutrophilsZebrafishLeukocyte L1 Antigen ComplexcalprotectincholeraIL-8innate immunityneutrophilsVibrio choleraezebrafish

Identifiers

PMID35072520
PMCPMC8929324
OpenAlexW4220899931

What OpenQuestion holds

Textmetadata
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.