Evidence map›Paper›PMID 22632124›Full record

ArticleCellular microbiology2012

Repression of bacterial lipoprotein production by Francisella novicida facilitates evasion of innate immune recognition.

Crystal L Jones, Timothy R Sampson, Helder I Nakaya, Bali Pulendran, David S Weiss

Abstract read
In one paragraph

Article in Cellular microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  10. The Involvement ofFrontiers in microbiology · 2021
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. RevisitingFrontiers in microbiology · 2018
    Article
  17. Journal of leukocyte biology · 2017
    Article
  18. Overview of CRISPR-Cas9 Biology.Cold Spring Harbor protocols · 2016
    Article
  19. Article
  20. Review
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 2 institutions in 1 country.

Crystal L JonesDepartment of Microbiology and Immunology, Microbiology and Molecular Genetics Program, Emory University, Atlanta, GA, USA.
Timothy R Sampson
Helder I Nakaya
Bali Pulendran
David S Weiss
Emory University · USEmory National Primate Research Center

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Yessinia autotransporters (Yaps): Structure, function, and host responseU54AI057157 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FROTHINGHAM, RICHARD · 2003 to 2013
$91.4M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Shop Module CoreP30EY008126 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Kevin L Schey · 1989 to 2026
$19.6M
VANTAGE:Consolidation to create the Vanderbilt Technologies for Advanced GenomicsG20RR030956 · NCRR · VANDERBILT UNIVERSITY · PI PIETENPOL, JENNIFER A · 2010 to 2010
$8.7M
ENNCF - Viral Vector CoreP30NS055077 · NINDS · EMORY UNIVERSITY · PI LEVEY, ALLAN I · 2008 to 2018
$6.8M
Modulation of host defenses by the bacterial pathogen Francisella tularensisR56AI087673 · NIAID · EMORY UNIVERSITY · PI WEISS, DAVID S · 2011 to 2011
$440k
NCI NIH HHS P30 CA068485NCI NIH HHS P30 CA68485NCRR NIH HHS G20 RR030956NEI NIH HHS P30 EY008126NEI NIH HHS P30 EY08126NIAID NIH HHS R56 AI087673NIAID NIH HHS U54 AI057157NIDDK NIH HHS P30 DK058404NIDDK NIH HHS P30 DK58404NINDS NIH HHS P30 NS055077NINDS NIH HHS P30NS055077
6 · The paper itself

Abstract

Innate recognition systems, including the Toll-like receptors (TLRs), play a critical role in activating host defences and proinflammatory pathways in response to infection. Pathogens have developed strategies to subvert TLRs in order to survive and replicate within the host. The model intracellular pathogen, Francisella novicida, modulates host defences to promote survival and replication in macrophages. TLR2, which recognizes bacterial lipoproteins (BLPs), is critical for activating host defences and proinflammatory cytokine production in response to Francisella infection. Here we show that the F. novicida protein FTN_0757 acts to repress BLP production, dampening TLR2 activation. The ΔFTN_0757 mutant strain induced robust TLR2-dependent cytokine production in macrophages compared with wild-type bacteria, and produced increased amounts of BLPs. The deletion of one BLP (FTN_1103) from ΔFTN_0757 decreased the total BLP concentration to near wild-type level sand correlated with a decrease in the inductionof TLR2 signalling. The overproduction of BLPs also contributed to the in vivo attenuation of the ΔFTN_0757 mutant, which was significantly rescued when FTN_1103 was deleted. Taken together, these data reveal a novel mechanism of immune evasion by the downregulation of BLP expression to subvert TLR2 activation, which is likely used by numerous other intracellular bacterial pathogens.

Indexed as

Immune EvasionAnimalsCells, CulturedCytokinesFrancisella tularensisGene DeletionLipoproteinsMacrophagesMiceRepressor ProteinsToll-Like Receptor 2VirulenceCytokinesLipoproteinsRepressor ProteinsTlr2 protein, mouseToll-Like Receptor 2

Identifiers

PMID22632124
PMCPMC3443312
OpenAlexW1897957811

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.