Evidence map›Paper›PMID 20596543›Full record

ArticlePloS one2010

Modeling susceptibility versus resistance in allergic airway disease reveals regulation by Tec kinase Itk.

Nisebita Sahu, J Luis Morales, Deborah Fowell, Avery August

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Therapeutic treatment of dietary docosahexaenoic acid for particle-induced pulmonary inflammation in Balb/c mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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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

4 authors at 2 institutions in 1 country.

Nisebita SahuCenter for Molecular Immunology and Infectious Disease and Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania, United States of America.
J Luis Morales
Deborah Fowell
Avery August
Pennsylvania State University · USUniversity of Rochester · US

Funding

Tyrosine Kinase ITK in Experimental Allergic AsthmaR01AI051626 · NIAID · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI AUGUST, AVERY · 2003 to 2012
$3.6M
Eosinophils and Allergic Airway ResponsesR01AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2012
$1.9M
The Role of Itk in Th DifferentiationR01AI050201 · NIAID · UNIVERSITY OF ROCHESTER · PI FOWELL, DEBORAH J · 2001 to 2005
$1.6M
ITK Mast Cells and Allergic Airway ResponsesR01AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2007 to 2011
$1.5M
ITK Mast Cells and Allergic Airway ResponsesR56AI065566 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2006 to 2006
$345k
Eosinophils and Allergic Airway ResponsesR56AI073955 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI AUGUST, AVERY · 2008 to 2008
$61k
NIAID NIH HHS AI051626NIAID NIH HHS AI065566NIAID NIH HHS AI073955NIAID NIH HHS R01 AI050201NIAID NIH HHS R01 AI051626NIAID NIH HHS R01 AI065566NIAID NIH HHS R01 AI073955NIAID NIH HHS R56 AI065566NIAID NIH HHS R56 AI073955
6 · The paper itself

Abstract

Murine models of allergic asthma have been used to understand the mechanisms of development and pathology in this disease. In addition, knockout mice have contributed significantly to our understanding of the roles of specific molecules and cytokines in these models. However, results can vary significantly depending on the mouse strain used in the model, and in particularly in understanding the effect of specific knockouts. For example, it can be equivocal as to whether specific gene knockouts affect the susceptibility of the mice to developing the disease, or lead to resistance. Here we used a house dust mite model of allergic airway inflammation to examine the response of two strains of mice (C57BL/6 and BALB/c) which differ in their responses in allergic airway inflammation. We demonstrate an algorithm that can facilitate the understanding of the behavior of these models with regards to susceptibility (to allergic airway inflammation) (S(aai)) or resistance (R(aai)) in this model. We verify that both C57BL/6 and BALB/c develop disease, but BALB/c mice have higher S(aai) for development. We then use this approach to show that the absence of the Tec family kinase Itk, which regulates the production of Th2 cytokines, leads to R(aai) in the C57BL/6 background, but decreases S(aai) on the BALB/c background. We suggest that the use of such approaches could clarify the behavior of various knockout mice in modeling allergic asthma.

Indexed as

Disease SusceptibilityAlgorithmsAnimalsBronchial HyperreactivityHypersensitivityMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutProtein-Tyrosine KinasesProtein-Tyrosine KinasesTec protein-tyrosine kinase

Identifiers

PMID20596543
PMCPMC2893210
OpenAlexW2015719017

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.