Evidence map›Paper›PMID 22901537›Full record

ArticleCell host & microbe2012

The Legionella pneumophila EnhC protein interferes with immunostimulatory muramyl peptide production to evade innate immunity.

Mingyu Liu, Eva Haenssler, Tsuyoshi Uehara, Vicki P Losick, James T Park, Ralph R Isberg

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. ACS infectious diseases · 2026
    Article
  2. Journal of bacteriology · 2024
    Review
  3. Protein sociology of ProA, Mip and other secreted virulence factors at theFrontiers in cellular and infection microbiology · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Recent Advances on the Innate Immune Response toFrontiers in cellular and infection microbiology · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Journal of bacteriology · 2019
    Article
  12. Article
  13. Epidemiological information is key when interpreting whole genome sequence data - lessons learned from a largeEuro surveillance : bulletin Europeen sur les maladies transmissibles = European communicable disease bulletin · 2017
    Article
  14. Review
  15. Article
  16. The SCID Mouse Model for Identifying Virulence Determinants inFrontiers in cellular and infection microbiology · 2017
    Article
  17. Article
  18. Article
  19. Review
  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

6 authors at 2 institutions in 1 country.

Mingyu LiuDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02115, USA.
Eva Haenssler
Tsuyoshi Uehara
Vicki P Losick
James T Park
Ralph R Isberg
Tufts University · USHoward Hughes Medical Institute · US

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Successful pathogens have evolved to evade innate immune recognition of microbial molecules by pattern recognition receptors (PRR), which control microbial growth in host tissues. Upon Legionella pneumophila infection of macrophages, the cytosolic PRR Nod1 recognizes anhydro-disaccharide-tetrapeptide (anhDSTP) generated by soluble lytic transglycosylase (SltL), the predominant bacterial peptidoglycan degrading enzyme, to activate NF-κB-dependent innate immune responses. We show that L. pneumophila periplasmic protein EnhC, which is uniquely required for bacterial replication within macrophages, interferes with SltL to lower anhDSTP production. L. pneumophila mutant strains lacking EnhC (ΔenhC) increase Nod1-dependent NF-κB activation in host cells, while reducing SltL activity in a ΔenhC strain restores intracellular bacterial growth. Further, L. pneumophila ΔenhC is specifically rescued in Nod1- but not Nod2-deficient macrophages, arguing that EnhC facilitates evasion from Nod1 recognition. These results indicate that a bacterial pathogen regulates peptidoglycan degradation to control the production of PRR ligands and evade innate immune recognition.

Indexed as

Immune EvasionBacterial ProteinsGlycosyltransferasesImmunity, InnateLegionella pneumophilaLegionnaires' DiseaseMacrophagesNF-kappa BNod1 Signaling Adaptor ProteinPeptidesBacterial ProteinsGlycosyltransferasesmurein transglycosylaseNF-kappa BNod1 Signaling Adaptor ProteinPeptides

Identifiers

PMID22901537
PMCPMC3678716
OpenAlexW1975320089

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.