Evidence map›Paper›PMID 19812196›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Regulation of gastric B cell recruitment is dependent on IL-17 receptor A signaling in a model of chronic bacterial infection.

Holly M Scott Algood, Shannon Sedberry Allen, Mary K Washington, Richard M Peek, Geraldine G Miller, Timothy L Cover

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 66 citations in OpenAlex.

  1. Managing dangerous liaisons: lessons fromJournal of bacteriology · 2026
    Review
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  9. Review
  10. T Cell Cytokines Impact Epithelial Cell Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020
    Review
  11. Frontiers in oncology · 2020
    Article
  12. Review
  13. Decreased IL-17RB expression impairs CD11bCell death & disease · 2019
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 3 countries.

Holly M Scott AlgoodVeterans Affairs Tennessee Valley Healthcare System, Nashville, TN 37212, USA. holly.m.algood@vanderbilt.edu
Shannon Sedberry Allen
Mary K Washington
Richard M Peek
Geraldine G Miller
Timothy L Cover
VA Tennessee Valley Healthcare System · USNational Institute of Pathology · INVanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Jin Chen · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Structure-function analysis of H. pylori VacAR01AI039657 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI TIMOTHY L COVER · 1996 to 2026
$8.3M
Helicobacter Pylori and Gastrointestinal BiologyR01DK058587 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PEEK, RICHARD M. · 2001 to 2024
$7.8M
Analysis of the H. Pylori cag pathogenicity islandR01AI068009 · NIAID · VANDERBILT UNIVERSITY · PI COVER, TIMOTHY L · 2008 to 2012
$1.9M
NCI NIH HHS P30 CA068485NCI NIH HHS P30 CA68485NIAID NIH HHS R01 AI039657NIAID NIH HHS R01 AI068009NIAID NIH HHS R01AI068009NIAID NIH HHS R01AI39657NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK058587NIDDK NIH HHS R0I DK58587
6 · The paper itself

Abstract

Th17-driven immune responses contribute to the pathogenesis of many chronic inflammatory diseases. In this study, we investigated the role of IL-17 signaling in chronic gastric inflammation induced by Helicobacter pylori, a Gram-negative bacterium that persistently colonizes the human stomach. Wild-type C57BL/6 mice and mice lacking IL-17RA (IL-17RA(-/-)) were orogastrically infected with H. pylori. Differences in bacterial colonization density and gastric inflammation were not apparent at 1 mo postinfection, but by 3 mo postinfection, H. pylori colonization density was higher and mononuclear gastric inflammation more severe in infected IL-17RA(-/-) mice than in infected wild-type mice. A striking feature was a marked increase in gastric B cells, plasma cells, and lymphoid follicles, along with enhanced H. pylori-specific serum Ab responses, in infected IL-17RA(-/-) mice. Fewer gastric neutrophils and lower levels of neutrophil-recruiting chemokines were detected in infected IL-17RA(-/-) mice than in infected wild-type mice. Gastric IL-17a and IL-21 transcript levels were significantly higher in infected IL-17RA(-/-) mice than in infected wild-type mice or uninfected mice, which suggested that a negative feedback loop was impaired in the IL-17RA(-/-) mice. These results underscore an important role of IL-17RA signaling in regulating B cell recruitment. In contrast to many chronic inflammatory diseases in which IL-17RA signaling promotes an inflammatory response, IL-17RA signaling down-regulates the chronic mononuclear inflammation elicited by H. pylori infection.

Indexed as

AnimalsB-Lymphocyte SubsetsCell Migration InhibitionCell MovementChronic DiseaseDisease Models, AnimalFemaleGastric MucosaHelicobacter InfectionsHelicobacter pyloriInflammation MediatorsInterleukin-17MaleMiceMice, Inbred C57BLMice, KnockoutIl17ra protein, mouseInflammation MediatorsInterleukin-17Receptors, Interleukin-17

Identifiers

PMID19812196
PMCPMC2834183
OpenAlexW2164114142

What OpenQuestion holds

Textmetadata
LicenceTDM
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.