Evidence map›Paper›PMID 21670171›Full record

ArticleInfection and immunity2011

A Francisella tularensis locus required for spermine responsiveness is necessary for virulence.

Brian C Russo, Joseph Horzempa, Dawn M O'Dee, Deanna M Schmitt, Matthew J Brown, Paul E Carlson, Ramnik J Xavier, Gerard J Nau

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 37 citations in OpenAlex.

  1. Spermidine biosynthesis by hypervirulentJournal of bacteriology · 2026
    Article
  2. Article
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  7. A predictedVirulence · 2019
    Article
  8. Article
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  12. Glycosylation of a Capsule-Like Complex (CLC) byFrontiers in microbiology · 2017
    Article
  13. Article
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  19. 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

8 authors at 2 institutions in 1 country.

Brian C RussoDepartment of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, 200 Lothrop St., Pittsburgh, PA 15261, USA.
Joseph Horzempa
Dawn M O'Dee
Deanna M Schmitt
Matthew J Brown
Paul E Carlson
Ramnik J Xavier
Gerard J Nau
University of Pittsburgh · USMassachusetts General Hospital · US

Funding

ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHRISTOPHER P DUGGAN · 1994 to 2026
$31.6M
Immunology of Infectious DiseaseT32AI060525 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI JoAnne L. Flynn · 2005 to 2026
$5.3M
Novel Selectable Markers for F. tularensisR21AI074402 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NAU, GERARD J · 2007 to 2008
$393k
NIAID NIH HHS AI074402NIAID NIH HHS R21 AI074402NIAID NIH HHS T32 AI060525NIDDK NIH HHS P30 DK040561
6 · The paper itself

Abstract

Tularemia is a debilitating febrile illness caused by the category A biodefense agent Francisella tularensis. This pathogen infects over 250 different hosts, has a low infectious dose, and causes high morbidity and mortality. Our understanding of the mechanisms by which F. tularensis senses and adapts to host environments is incomplete. Polyamines, including spermine, regulate the interactions of F. tularensis with host cells. However, it is not known whether responsiveness to polyamines is necessary for the virulence of the organism. Through transposon mutagenesis of F. tularensis subsp. holarctica live vaccine strain (LVS), we identified FTL_0883 as a gene important for spermine responsiveness. In-frame deletion mutants of FTL_0883 and FTT_0615c, the homologue of FTL_0883 in F. tularensis subsp. tularensis Schu S4 (Schu S4), elicited higher levels of cytokines from human and murine macrophages compared to wild-type strains. Although deletion of FTL_0883 attenuated LVS replication within macrophages in vitro, the Schu S4 mutant with a deletion in FTT_0615c replicated similarly to wild-type Schu S4. Nevertheless, both the LVS and the Schu S4 mutants were significantly attenuated in vivo. Growth and dissemination of the Schu S4 mutant was severely reduced in the murine model of pneumonic tularemia. This attenuation depended on host responses to elevated levels of proinflammatory cytokines. These data associate responsiveness to polyamines with tularemia pathogenesis and define FTL_0883/FTT_0615c as an F. tularensis gene important for virulence and evasion of the host immune response.

Indexed as

AnimalsBacterial ProteinsCells, CulturedChemokinesCytokinesEnzyme-Linked Immunosorbent AssayFemaleFrancisella tularensisHost-Pathogen InteractionsHumansMacrophagesMiceMice, Inbred C57BLMutagenesisPolymerase Chain ReactionSequence DeletionBacterial ProteinsChemokinesCytokinesSpermine

Identifiers

PMID21670171
PMCPMC3165480
OpenAlexW2129609057

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.