Evidence map›Paper›PMID 20195507›Full record

ArticlePLoS pathogens2010

Transit through the flea vector induces a pretransmission innate immunity resistance phenotype in Yersinia pestis.

Viveka Vadyvaloo, Clayton Jarrett, Daniel E Sturdevant, Florent Sebbane, B Joseph Hinnebusch

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.6field-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

84 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
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  8. Article
  9. Role of themBio · 2024
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  12. CsrA-Mediated Translational Activation of theJournal of bacteriology · 2023
    Article
  13. Zoonoses (Shannon, Ireland) · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. ACS infectious diseases · 2021
    Article
  18. Article
  19. Review
  20. Review

24 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

5 authors at 4 institutions in 3 countries.

Viveka VadyvalooLaboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, United States of America.
Clayton Jarrett
Daniel E Sturdevant
Florent Sebbane
B Joseph Hinnebusch
National Institutes of Health · USGenomics (United Kingdom) · GBNational Institute of Allergy and Infectious Diseases · USUniversité Lille Nord de France · FR

Funding

Transmission Of Yersinia Pestis By Fleas: Molecular MechanismsZIAAI000796 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HINNEBUSCH, B J · 2009 to 2023
$9.7M
Intramural NIH HHS
6 · The paper itself

Abstract

Yersinia pestis, the agent of plague, is transmitted to mammals by infected fleas. Y. pestis exhibits a distinct life stage in the flea, where it grows in the form of a cohesive biofilm that promotes transmission. After transmission, the temperature shift to 37 degrees C induces many known virulence factors of Y. pestis that confer resistance to innate immunity. These factors are not produced in the low-temperature environment of the flea, however, suggesting that Y. pestis is vulnerable to the initial encounter with innate immune cells at the flea bite site. In this study, we used whole-genome microarrays to compare the Y. pestis in vivo transcriptome in infective fleas to in vitro transcriptomes in temperature-matched biofilm and planktonic cultures, and to the previously characterized in vivo gene expression profile in the rat bubo. In addition to genes involved in metabolic adaptation to the flea gut and biofilm formation, several genes with known or predicted roles in resistance to innate immunity and pathogenicity in the mammal were upregulated in the flea. Y. pestis from infected fleas were more resistant to phagocytosis by macrophages than in vitro-grown bacteria, in part attributable to a cluster of insecticidal-like toxin genes that were highly expressed only in the flea. Our results suggest that transit through the flea vector induces a phenotype that enhances survival and dissemination of Y. pestis after transmission to the mammalian host.

Indexed as

BiofilmsAdaptation, PhysiologicalAnimalsGene ExpressionGene Expression ProfilingGenes, BacterialImmunity, InnateInsect VectorsOligonucleotide Array Sequence AnalysisPhenotypeReverse Transcriptase Polymerase Chain ReactionSiphonapteraYersinia pestis

Identifiers

PMID20195507
PMCPMC2829055
OpenAlexW2107111524

What OpenQuestion holds

Textmetadata
LicenceCC0
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.