Evidence map›Paper›PMID 18007012›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2008

Aryl hydrocarbon receptor targets pathways extrinsic to bone marrow cells to enhance neutrophil recruitment during influenza virus infection.

Sabine Teske, Andrea A Bohn, Jason P Hogaboam, B Paige Lawrence

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

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  13. Differential consequences of two distinct AhR ligands on innate and adaptive immune responses to influenza A virus.Toxicological sciences : an official journal of the Society of Toxicology · 2014
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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 1 institution in 1 country.

Sabine TeskeDepartment of Pharmaceutical Sciences and Pharmacology/Toxicology Graduate Program, College of Pharmacy, Washington State University, Pullman 99164, USA.
Andrea A Bohn
Jason P Hogaboam
B Paige Lawrence
Washington State University · US

Funding

TRAINING IN BIOTECHNOLOGY: EMPHASIS ON PROTEIN CHEMISTRYT32GM008336 · NIGMS · WASHINGTON STATE UNIVERSITY · PI CALL, DOUGLAS R. · 1989 to 2023
$8.9M
MECHANISMS OF TCDD PULMONARY IMMUNOTOXICITYR01ES010619 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B. PAIGE · 2000 to 2004
$1.2M
Mechanisms by which TCDD impairs immunological memoryK02ES012409 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B PAIGE · 2005 to 2009
$619k
NIEHS NIH HHS K02 ES012409NIEHS NIH HHS K02-ES012409NIEHS NIH HHS R01 ES010619NIEHS NIH HHS R01-ES10619NIGMS NIH HHS T32 GM008336NIGMS NIH HHS T32-GM008336
6 · The paper itself

Abstract

There is growing evidence that neutrophils influence host resistance during influenza virus infection; however, factors that regulate neutrophil migration to the lung during viral infection are unclear. Activation of the aryl hydrocarbon receptor (AhR) by the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) results in an increased number of neutrophils in the lung after influenza virus infection. The mechanism of AhR-mediated neutrophilia does not involve elevated levels of soluble neutrophil chemoattractants, upregulated adhesion molecules on pulmonary neutrophils, delayed neutrophil apoptosis, or increased vascular damage. In this study, we determined whether AhR activation increases neutrophil numbers systemically or only in the infected lung, and whether AhR-regulated events within the hematopoietic system underlie the dioxin-induced increase in pulmonary neutrophils observed during influenza virus infection. We report here that AhR activation does not increase neutrophil numbers systemically or increase neutrophil production in hematopoietic tissue, suggesting that the elevated number of neutrophils is restricted to the site of antigen challenge. The generation of CD45.2AhR-/--->CD45.1AhR+/+ bone marrow chimeric mice demonstrates that even when hematopoietic cells lack the AhR, TCDD treatment still results in twice as many pulmonary neutrophils compared with control-treated, infected CD45.2AhR-/--->CD45.1AhR+/+ chimeric mice. This finding reveals that AhR-mediated events extrinsic to bone marrow-derived cells affect the directional migration of neutrophils to the infected lung. These results suggest that the lung contains important and heretofore overlooked targets of AhR regulation, unveiling a novel mechanism for controlling neutrophil recruitment to the infected lung.

Indexed as

Influenza A Virus, H3N2 SubtypeNeutrophil InfiltrationAnimalsBasic Helix-Loop-Helix ProteinsBone Marrow CellsBronchoalveolar Lavage FluidChimeraDisease Models, AnimalEnvironmental PollutantsFemaleLeukocyte Common AntigensLungMiceMice, Inbred C57BLMice, KnockoutNeutrophilsAhr protein, mouseBasic Helix-Loop-Helix ProteinsEnvironmental PollutantsLeukocyte Common AntigensPolychlorinated DibenzodioxinsPtprc protein, mouseReceptors, Aryl Hydrocarbon

Identifiers

PMID18007012
PMCPMC2919339
OpenAlexW2165245693

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.