Evidence map›Paper›PMID 26177454›Full record

ArticlePloS one2015

Resistance to Innate Immunity Contributes to Colonization of the Insect Gut by Yersinia pestis.

Shaun C Earl, Miles T Rogers, Jennifer Keen, David M Bland, Andrew S Houppert, Caitlynn Miller, Ian Temple, Deborah M Anderson, Melanie M Marketon

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
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  7. ACS infectious diseases · 2021
    Article
  8. Review
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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

9 authors.

Shaun C EarlDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
Miles T RogersDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
Jennifer KeenDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
David M BlandDepartment of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, United States of America.
Andrew S HouppertDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
Caitlynn MillerDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
Ian TempleDepartment of Biology, Indiana University, Bloomington, IN, United States of America.
Deborah M AndersonDepartment of Veterinary Pathobiology, University of Missouri, Columbia, Missouri, United States of America.
Melanie M MarketonDepartment of Biology, Indiana University, Bloomington, IN, United States of America.

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Development of a Drosophila model to study vector colonization by Yersinia pestisR21AI101242 · NIAID · TRUSTEES OF INDIANA UNIVERSITY · PI MARKETON, MELANIE · 2013 to 2014
$439k
NIAID NIH HHS R21 AI101242NIAID NIH HHS R21AI101242NIH HHS P40 OD018537NIH HHS P40OD018537
6 · The paper itself

Abstract

Yersinia pestis, the causative agent of bubonic and pneumonic plague, is typically a zoonotic vector-borne disease of wild rodents. Bacterial biofilm formation in the proventriculus of the flea contributes to chronic infection of fleas and facilitates efficient disease transmission. However prior to biofilm formation, ingested bacteria must survive within the flea midgut, and yet little is known about vector-pathogen interactions that are required for flea gut colonization. Here we establish a Drosophila melanogaster model system to gain insight into Y. pestis colonization of the insect vector. We show that Y. pestis establishes a stable infection in the anterior midgut of fly larvae, and we used this model system to study the roles of genes involved in biofilm production and/or resistance to gut immunity stressors. We find that PhoP and GmhA both contribute to colonization and resistance to antimicrobial peptides in flies, and furthermore, the data suggest biofilm formation may afford protection against antimicrobial peptides. Production of reactive oxygen species in the fly gut, as in fleas, also serves to limit bacterial infection, and OxyR mediates Y. pestis survival in both insect models. Overall, our data establish the fruit fly as an informative model to elucidate the relationship between Y. pestis and its flea vector.

Indexed as

Immunity, InnateAnimalsAntimicrobial Cationic PeptidesBiofilmsColony Count, MicrobialDigestive SystemDisease ResistanceDrosophila melanogasterLarvaMutationReactive Oxygen SpeciesSiphonapteraYersinia pestisAntimicrobial Cationic PeptidesReactive Oxygen Species

Identifiers

PMID26177454
PMCPMC4503695

What OpenQuestion holds

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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.