Evidence map›Paper›PMID 24692449›Full record

ArticleeLife2014

Bacterial autolysins trim cell surface peptidoglycan to prevent detection by the Drosophila innate immune system.

Magda Luciana Atilano, Pedro Matos Pereira, Filipa Vaz, Maria João Catalão, Patricia Reed, Inês Ramos Grilo, Rita Gonçalves Sobral, Petros Ligoxygakis, Mariana Gomes Pinho, Sérgio Raposo Filipe

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 2 institutions in 2 countries.

Magda Luciana AtilanoLaboratory of Bacterial Cell Surfaces and Pathogenesis, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Pedro Matos PereiraLaboratory of Bacterial Cell Biology, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Filipa VazLaboratory of Bacterial Cell Surfaces and Pathogenesis, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Maria João CatalãoLaboratory of Bacterial Cell Surfaces and Pathogenesis, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Patricia ReedLaboratory of Bacterial Cell Biology, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Inês Ramos GriloLaboratory of Molecular Genetics, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Rita Gonçalves SobralDepartamento de Ciências da Vida, Centro de Recursos Microbiologicos (CREM), Faculdade de Ciências e Tecnologia, Universidade Nova de Lisboa, Caparica, Portugal.
Petros LigoxygakisGenes and Development Laboratory, Department of Biochemistry, University of Oxford, Oxford, United Kingdom.
Mariana Gomes PinhoLaboratory of Bacterial Cell Biology, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Sérgio Raposo FilipeLaboratory of Bacterial Cell Surfaces and Pathogenesis, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa (ITQB-UNL), Oeiras, Portugal.
Universidade Nova de Lisboa · PTUniversity of Oxford · GB

Funding

European Research Council 310987Medical Research Council G0300170Wellcome TrustWellcome Trust WT087680
6 · The paper itself

Abstract

Bacteria have to avoid recognition by the host immune system in order to establish a successful infection. Peptidoglycan, the principal constituent of virtually all bacterial surfaces, is a specific molecular signature recognized by dedicated host receptors, present in animals and plants, which trigger an immune response. Here we report that autolysins from Gram-positive pathogenic bacteria, enzymes capable of hydrolyzing peptidoglycan, have a major role in concealing this inflammatory molecule from Drosophila peptidoglycan recognition proteins (PGRPs). We show that autolysins trim the outermost peptidoglycan fragments and that in their absence bacterial virulence is impaired, as PGRPs can directly recognize leftover peptidoglycan extending beyond the external layers of bacterial proteins and polysaccharides. The activity of autolysins is not restricted to the producer cells but can also alter the surface of neighboring bacteria, facilitating the survival of the entire population in the infected host. DOI: http://dx.doi.org/10.7554/eLife.02277.001.

Indexed as

Immunity, InnateAnimalsDrosophilaGram-Positive BacteriaHydrolysisN-Acetylmuramoyl-L-alanine AmidasePeptidoglycanVirulenceN-Acetylmuramoyl-L-alanine AmidasePeptidoglycanbacterial infectionpeptidoglycanpeptidoglycan hydrolasesPGRPStaphylococcus aureusStreptococcus pneumoniae

Identifiers

PMID24692449
PMCPMC3971415
OpenAlexW2141962740

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.