Evidence map›Paper›PMID 24478091›Full record

ArticleInfection and immunity2014

G proteins Gαi1/3 are critical targets for Bordetella pertussis toxin-induced vasoactive amine sensitization.

Sean A Diehl, Benjamin McElvany, Rajkumar Noubade, Nathan Seeberger, Brock Harding, Karen Spach, Cory Teuscher

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. DAT, deacylating autotransporter toxin, fromProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  3. Article
  4. Article
  5. Gene Expression Profiling of Type 2 Diabetes Mellitus by Bioinformatics Analysis.Computational and mathematical methods in medicine · 2020
    Article
  6. Review
  7. Review
  8. Article
  9. 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

7 authors at 1 institution in 1 country.

Sean A DiehlDepartment of Medicine-Infectious Diseases, University of Vermont College of Medicine, Burlington, Vermont, USA.
Benjamin McElvany
Rajkumar Noubade
Nathan Seeberger
Brock Harding
Karen Spach
Cory Teuscher
University of Vermont · US

Funding

Susceptibilty and Resistance Loci in Mouse EAER01NS036526 · NINDS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI TEUSCHER, CORY · 1996 to 2008
$4.4M
Histamine Receptor Signaling in CNS Autoimmune DiseaseR01NS061014 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2008 to 2012
$3.1M
H1R Signaling and Immune Deviation in EAER01NS069628 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TEUSCHER, CORY · 2010 to 2014
$1.6M
NINDS NIH HHS NS061014NINDS NIH HHS NS069628NINDS NIH HHS NS36526NINDS NIH HHS R01 NS036526NINDS NIH HHS R01 NS061014NINDS NIH HHS R01 NS069628
6 · The paper itself

Abstract

Pertussis toxin (PTX) is an AB5-type exotoxin produced by the bacterium Bordetella pertussis, the causative agent of whooping cough. In vivo intoxication with PTX elicits a variety of immunologic and inflammatory responses, including vasoactive amine sensitization (VAAS) to histamine (HA), serotonin (5-HT), and bradykinin (BDK). Previously, by using a forward genetic approach, we identified the HA H1 receptor (Hrh1/H1R) as the gene in mice that controls differential susceptibility to B. pertussis PTX-induced HA sensitization (Bphs). Here we show, by using inbred strains of mice, F1 hybrids, and segregating populations, that, unlike Bphs, PTX-induced 5-HT sensitivity (Bpss) and BDK sensitivity (Bpbs) are recessive traits and are separately controlled by multiple loci unlinked to 5-HT and BDK receptors, respectively. Furthermore, we found that PTX sensitizes mice to HA independently of Toll-like receptor 4, a purported receptor for PTX, and that the VAAS properties of PTX are not dependent upon endothelial caveolae or endothelial nitric oxide synthase. Finally, by using mice deficient in individual Gαi/o G-protein subunits, we demonstrate that Gαi1 and Gαi3 are the critical in vivo targets of ADP-ribosylation underlying VAAS elicited by PTX exposure.

Indexed as

Adenosine Diphosphate RiboseAminesAnimalsBordetella pertussisCardiovascular AgentsGTP-Binding Protein alpha Subunits, Gi-GoMiceMice, KnockoutPertussis ToxinAdenosine Diphosphate RiboseAminesCardiovascular AgentsGnai1 protein, mouseGnai3 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoPertussis Toxin

Identifiers

PMID24478091
PMCPMC3911370
OpenAlexW2157032204

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.