Evidence map›Paper›PMID 34887398›Full record

ArticleNature communications2021

Population analysis of Legionella pneumophila reveals a basis for resistance to complement-mediated killing.

Bryan A Wee, Joana Alves, Diane S J Lindsay, Ann-Brit Klatt, Fiona A Sargison, Ross L Cameron, Amy Pickering, Jamie Gorzynski, Jukka Corander, Pekka Marttinen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Pathogens (Basel, Switzerland) · 2026
    Article
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  3. The discovery of aScience advances · 2025
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  5. mBio · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Lipopolysaccharide ofInternational journal of molecular sciences · 2023
    Article
  12. Article
  13. Article
  14. A Tale of Four Danish Cities:International journal of environmental research and public health · 2022
    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

13 authors at 6 institutions in 4 countries.

Bryan A Wee *The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0001-6135-5903
Joana Alves *The Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0003-3131-9834
Diane S J LindsayBacterial Respiratory Infections Service (Ex Mycobacteria), Scottish Microbiology Reference Laboratory, Glasgow, Scotland, UK.ORCID http://orcid.org/0000-0003-1378-0926
Ann-Brit KlattDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.
Fiona A SargisonThe Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0001-5160-4208
Ross L CameronNHS National Services Scotland, Health Protection Scotland, Glasgow, Scotland, UK.
Amy PickeringThe Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0003-2154-224X
Jamie GorzynskiThe Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK.ORCID http://orcid.org/0000-0002-4921-9789
Jukka CoranderDepartment of Mathematics and Statistics, University of Helsinki, Helsinki, Finland.
Pekka MarttinenHelsinki Institute for Information Technology, Department of Computer Science, Aalto University, Aalto, Finland.ORCID http://orcid.org/0000-0001-7078-7927
Bastian OpitzDepartment of Internal Medicine/Infectious Diseases and Pulmonary Medicine, Charité Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0003-1276-836X
Andrew J SmithBacterial Respiratory Infections Service (Ex Mycobacteria), Scottish Microbiology Reference Laboratory, Glasgow, Scotland, UK.ORCID http://orcid.org/0000-0003-0580-4078
J Ross FitzgeraldThe Roslin Institute, Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, Scotland, UK. Ross.Fitzgerald@ed.ac.uk.ORCID http://orcid.org/0000-0002-9233-8468
Roslin Institute · GBCharité - Universitätsmedizin Berlin · DEHealth Protection Scotland · GBHelsinki Institute for Information Technology · FIStatistics Finland · FIUniversity of Glasgow · GB

Funding

Biotechnology and Biological Sciences Research Council BB/P013740/1Chief Scientist Office ETM/421Chief Scientist Office (CSO) ETM/421Medical Research Council MR/L015080/1Medical Research Council MR/N02995X/1Wellcome Trust 201531/Z/16/ZWellcome Trust (Wellcome) 201531/Z/16/Z
6 · The paper itself

Abstract

Legionella pneumophila is the most common cause of the severe respiratory infection known as Legionnaires' disease. However, the microorganism is typically a symbiont of free-living amoeba, and our understanding of the bacterial factors that determine human pathogenicity is limited. Here we carried out a population genomic study of 902 L. pneumophila isolates from human clinical and environmental samples to examine their genetic diversity, global distribution and the basis for human pathogenicity. We find that the capacity for human disease is representative of the breadth of species diversity although some clones are more commonly associated with clinical infections. We identified a single gene (lag-1) to be most strongly associated with clinical isolates. lag-1, which encodes an O-acetyltransferase for lipopolysaccharide modification, has been distributed horizontally across all major phylogenetic clades of L. pneumophila by frequent recent recombination events. The gene confers resistance to complement-mediated killing in human serum by inhibiting deposition of classical pathway molecules on the bacterial surface. Furthermore, acquisition of lag-1 inhibits complement-dependent phagocytosis by human neutrophils, and promoted survival in a mouse model of pulmonary legionellosis. Thus, our results reveal L. pneumophila genetic traits linked to disease and provide a molecular basis for resistance to complement-mediated killing.

Indexed as

AcetyltransferasesAnimalsBacterial ProteinsComplement System ProteinsFemaleGenome, BacterialHumansLegionella pneumophilaLegionnaires' DiseaseMiceMice, Inbred C57BLNeutrophilsPhylogenyAcetyltransferasesBacterial ProteinsComplement System Proteins

Identifiers

PMID34887398
PMCPMC8660822
OpenAlexW4200576288

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.