Evidence map›Paper›PMID 22547547›Full record

ArticleInfection and immunity2012

NOD2 signaling contributes to host defense in the lungs against Escherichia coli infection.

Balamayooran Theivanthiran, Sanjay Batra, Gayathriy Balamayooran, Shanshan Cai, Koichi Kobayashi, Richard A Flavell, Samithamby Jeyaseelan

RetractedErratum issuedOpen access · bronzeAbstract readRetracted Publication
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Nod2: The intestinal gate keeper.PLoS pathogens · 2017
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. The role of NOD2 in murine and human melioidosis.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Article
  17. Review
  18. Article
  19. NOD-Like Receptors in Lung Diseases.Frontiers in immunology · 2013
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Balamayooran TheivanthiranLaboratory of Lung Biology, Department of Pathobiological Sciences and Center for Experimental Infectious Disease Research, Harvard Medical School, Boston, Massachusetts, USA.
Sanjay Batra
Gayathriy Balamayooran
Shanshan Cai
Koichi Kobayashi
Richard A Flavell
Samithamby Jeyaseelan
Dana-Farber Cancer Institute · USHoward Hughes Medical Institute · USLouisiana State University Health Sciences Center New Orleans · US

Funding

Neutrophil Accumulation in Bacterial PneumoniaR01HL091958 · NHLBI · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI JEYASEELAN, SAMITHAMBY · 2008 to 2017
$3.8M
NHLBI NIH HHS R01 HL-091958NHLBI NIH HHS R01 HL091958NHLBI NIH HHS R01 HL-091958S1
6 · The paper itself

Abstract

Bacterial pneumonia remains a significant cause of mortality in the United States. The innate immune response is the first line of defense against invading bacteria. Neutrophil recruitment to the lungs is the first step in a multistep sequence leading to bacterial clearance. Ligand interaction with pattern-recognizing receptors (PRRs) leads to chemokine production, which drives neutrophils to the site of infection. Although we demonstrated that RIP2 is important for host defense in the lungs against Escherichia coli, the individual roles of NOD1 and NOD2 in pulmonary defense have not been addressed. Here, we explored the role of NOD2 in neutrophil-mediated host defense against an extracellular pathogen, E. coli. We found enhanced bacterial burden and reduced neutrophil and cytokine/chemokine levels in the lungs of NOD2⁻/⁻ mice following E. coli infection. Furthermore, we observed reduced activation of NF-κB and mitogen-activated protein kinases (MAPKs) in the lungs of NOD2⁻/⁻ mice upon E. coli challenge. Moreover, NOD2⁻/⁻ neutrophils show impaired intracellular bacterial killing. Using NOD2/RIP2⁻/⁻ mice, we observed bacterial burden and neutrophil accumulation in the lungs similar to those seen with NOD2⁻/⁻ mice. In addition, bone marrow-derived macrophages obtained from NOD2/RIP2⁻/⁻ mice demonstrate a reduction in activation of NF-κB and MAPKs similar to that seen with NOD2⁻/⁻ mice in response to E. coli. These findings unveil a previously unrecognized role of the NOD2-RIP2 axis for host defense against extracellular Gram-negative bacteria. This pathway may represent a novel target for the treatment of lung infection/inflammation.

Indexed as

Signal TransductionAnimalsBacterial LoadCytokinesEscherichia coli InfectionsFemaleLungMiceMice, Inbred C57BLNeutrophilsNod2 Signaling Adaptor ProteinPneumonia, BacterialReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesCytokinesNod2 protein, mouseNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouse

Identifiers

PMID22547547
PMCPMC3416478
OpenAlexW2129237473

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.