Evidence map›Paper›PMID 19759900›Full record

ArticlePloS one2009

Pertussis toxin stimulates IL-17 production in response to Bordetella pertussis infection in mice.

Charlotte Andreasen, Daniel A Powell, Nicholas H Carbonetti

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 110 citations in OpenAlex.

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  10. DNA-Dependent Interferon Induction and Lung Inflammation inJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2023
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  13. Conquering the host:Frontiers in microbiology · 2022
    Review
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  20. DisruptingMicroorganisms · 2020
    Article

14 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Charlotte AndreasenDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD, USA.
Daniel A Powell
Nicholas H Carbonetti
University of Maryland, Baltimore · US

Funding

Role of Pertussis Toxin in Bordetella pertussis infectionR01AI063080 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI CARBONETTI, NICHOLAS H · 2006 to 2010
$1.9M
NIAID NIH HHS R01 AI063080
6 · The paper itself

Abstract

In a mouse model of respiratory tract infection by Bordetella pertussis, bacteria multiply in the airways over the first week and are then cleared over the next 3-4 weeks by the host immune response. Pertussis toxin (PT), a virulence factor secreted exclusively by B. pertussis, promotes bacterial growth in the airways by suppression and modulation of host immune responses. By comparison of wild type and PT-deficient strains, we examined the role of PT in modulating airway cytokine and chemokine responses affecting neutrophil recruitment during B. pertussis infection in mice. We found that, despite early inhibition of neutrophil recruitment by PT, high numbers of neutrophils were recruited to the airways by 4 days post-infection with the wild type strain, but not with the PT-deficient strain, and that this correlated with upregulation of neutrophil-attracting chemokine gene expression. In addition, there was similar upregulation of genes expressing the cytokines IL-17A (IL-17), TNF-alpha and IFN-gamma, indicating a mixed Th1/Th17 response. Expression of IL-6, a cytokine involved in Th17 induction, was upregulated earlier than the IL-17 response. We showed that PT, rather than bacterial numbers, was important for induction of these responses. Flow cytometric analysis revealed that the IL-17-producing cells were macrophages and neutrophils as well as T cells, and were present predominantly in the airways rather than the lung tissue. Antibody neutralization of IL-17 significantly reduced chemokine gene expression and neutrophil recruitment to the airways, but only modestly increased peak bacterial loads. These data indicate that PT stimulates inflammatory responses by induction of Th1- and Th17-associated cytokines, including IL-17, during B. pertussis infection in mice, but a role for IL-17 in protection against the infection remains to be established.

Indexed as

Gene Expression Regulation, BacterialAnimalsBordetella pertussisGene Expression ProfilingInterferon-gammaInterleukin-17KineticsMiceNeutrophilsPertussis ToxinTh1 CellsTumor Necrosis Factor-alphaVirulence FactorsWhooping CoughInterferon-gammaInterleukin-17Pertussis ToxinTumor Necrosis Factor-alphaVirulence Factors

Identifiers

PMID19759900
PMCPMC2738961
OpenAlexW2055254020

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.