Evidence map›Paper›PMID 22106256›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Bacterial chemotaxis modulates host cell apoptosis to establish a T-helper cell, type 17 (Th17)-dominant immune response in Helicobacter pylori infection.

Annah S Rolig, J Elliot Carter, Karen M Ottemann

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 47 citations in OpenAlex.

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  12. SalmoNet, an integrated network of tenNPJ systems biology and applications · 2017
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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

3 authors at 2 institutions in 1 country.

Annah S RoligDepartment of Molecular, Cellular, and Developmental Biology, University of California, Santa Cruz, CA 95064, USA.
J Elliot Carter
Karen M Ottemann
University of California, Santa Cruz · USUniversity of South Alabama · US

Funding

Roles for Motility in Helicobactor pylori pathogenesisR01AI050000 · NIAID · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI OTTEMANN, KAREN M · 2002 to 2011
$3.6M
NIAID NIH HHS AI050000NIAID NIH HHS R01 AI050000
6 · The paper itself

Abstract

The host inflammatory response to chronic bacterial infections often dictates the disease outcome. In the case of the gastric pathogen Helicobacter pylori, host inflammatory responses result in outcomes that range from moderate and asymptomatic to more severe with concomitant ulcer or cancers. It was found recently that H. pylori chemotaxis mutants (Che(-)), which lack directed motility but colonize to nearly wild-type levels, trigger less host inflammation. We used these mutants to observe host immune responses that resulted in reduced disease states. Here we report that these mutants are defective for early gastric recruitment of CD4(+) T cells compared with wild-type infection. Furthermore, Che(-) mutant infections lack the T-helper cell, type 17 (Th17) component of the immune response, as measured by cytokine mRNA levels in gastric tissue via intracellular cytokine staining and immunofluorescence. We additionally find that a Che(-) mutant infection results in significantly less host cell apoptosis than does wild-type infection, in accordance with previous observations that T-helper cell, type 17 responses in Citrobacter rodentium infections are driven by concomitant bacterial and apoptotic cell signals. We propose that bacterial chemotaxis allows H. pylori to access a particular host niche that allows the bacteria to express or deliver proapoptotic host cell factors. This report indicates that chemotaxis plays a role in enhancing apoptosis, suggesting bacterial chemotaxis systems might serve as therapeutic targets for infections whose symptoms arise from host cell apoptosis and tissue damage.

Indexed as

AnimalsApoptosisBacterial Physiological PhenomenaBacterial ProteinsCD4-Positive T-LymphocytesCitrobacter rodentiumCoinfectionCytokinesEnterobacteriaceae InfectionsFemaleFlow CytometryGastric MucosaGastritisHelicobacter InfectionsHelicobacter pyloriHost-Pathogen InteractionsBacterial ProteinsCytokinesMembrane ProteinsMethyl-Accepting Chemotaxis Proteins

Identifiers

PMID22106256
PMCPMC3241786
OpenAlexW1981877126

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.