Evidence map›Paper›PMID 22654100›Full record

ArticleThe Journal of biological chemistry2012

Identification of a novel Francisella tularensis factor required for intramacrophage survival and subversion of innate immune response.

Manish Mahawar, Maninjay K Atianand, Rachel J Dotson, Vanessa Mora, Seham M Rabadi, Dennis W Metzger, Jason F Huntley, Jonathan A Harton, Meenakshi Malik, Chandra Shekhar Bakshi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Cells · 2023
    Article
  3. Identification ofFrontiers in cellular and infection microbiology · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Journal of bioterrorism & biodefense · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 4 institutions in 1 country.

Manish MahawarCenter for Immunology and Microbial Disease, Albany Medical College, Albany, New York 12208, USA.
Maninjay K Atianand
Rachel J Dotson
Vanessa Mora
Seham M Rabadi
Dennis W Metzger
Jason F Huntley
Jonathan A Harton
Meenakshi Malik
Chandra Shekhar Bakshi
Albany Medical Center Hospital · USNew York Medical College · USAlbany College of Pharmacy and Health Sciences · USUniversity of Toledo Medical Center · US

Funding

TLR2/NLR Signal Regulation of Protective Immunity to F. TularensisP01AI056320 · NIAID · ALBANY MEDICAL COLLEGE · PI METZGER, DENNIS W · 2003 to 2016
$22.9M
Synergistic extra and intracellular recognition of F. tularensisR21AI075250 · NIAID · ALBANY MEDICAL COLLEGE · PI MALIK, MEENAKSHI · 2009 to 2010
$430k
Modulation of macrophage function by Francisella tularensisR56AI090072 · NIAID · NEW YORK MEDICAL COLLEGE · PI BAKSHI, CHANDRA SHEKHAR · 2010 to 2010
$316k
NIAID NIH HHS 1R21AI075250-01A2NIAID NIH HHS 2P01AI056320NIAID NIH HHS 7R56AI090072-02NIAID NIH HHS P01 AI056320NIAID NIH HHS R21 AI075250NIAID NIH HHS R56 AI090072
6 · The paper itself

Abstract

Francisella tularensis, the causative agent of tularemia, is one of the deadliest agents of biological warfare and bioterrorism. Extremely high virulence of this bacterium is associated with its ability to dampen or subvert host innate immune response. The objectives of this study were to identify factors and understand the mechanisms of host innate immune evasion by F. tularensis. We identified and explored the pathogenic role of a mutant interrupted at gene locus FTL_0325, which encodes an OmpA-like protein. Our results establish a pathogenic role of FTL_0325 and its ortholog FTT0831c in the virulent F. tularensis SchuS4 strain in intramacrophage survival and suppression of proinflammatory cytokine responses. This study provides mechanistic evidence that the suppressive effects on innate immune responses are due specifically to these proteins and that FTL_0325 and FTT0831c mediate immune subversion by interfering with NF-κB signaling. Furthermore, FTT0831c inhibits NF-κB activity primarily by preventing the nuclear translocation of p65 subunit. Collectively, this study reports a novel F. tularensis factor that is required for innate immune subversion caused by this deadly bacterium.

Indexed as

Immunity, InnateAnimalsBacterial Outer Membrane ProteinsCell LineFrancisella tularensisGenetic LociHumansMacrophagesMiceMice, Inbred BALB CSignal TransductionTranscription Factor RelATularemiaVirulence FactorsBacterial Outer Membrane ProteinsRELA protein, humanRela protein, mouseTranscription Factor RelAVirulence Factors

Identifiers

PMID22654100
PMCPMC3408198
OpenAlexW2008060164

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.