Evidence map›Paper›PMID 32220647›Full record

ArticleCell host & microbe2020

Paradoxical Pro-inflammatory Responses by Human Macrophages to an Amoebae Host-Adapted Legionella Effector.

Christopher Price, Snake Jones, Mirna Mihelcic, Marina Santic, Yousef Abu Kwaik

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026
    Review
  4. Article
  5. Article
  6. Integrated Molecular Diagnostics UnmaskInfection and drug resistance · 2025
    Article
  7. Frontiers in cellular and infection microbiology · 2025
    Article
  8. Journal of bacteriology · 2024
    Review
  9. Article
  10. Review
  11. Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  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

5 authors at 2 institutions in 2 countries.

Christopher PriceDepartment of Microbiology and Immunology, College of Medicine, University of Louisville, Louisville, KY, USA.
Snake JonesDepartment of Microbiology and Immunology, College of Medicine, University of Louisville, Louisville, KY, USA.
Mirna MihelcicUniversity of Rijeka, Rijeka, Croatia.
Marina SanticUniversity of Rijeka, Rijeka, Croatia.
Yousef Abu KwaikDepartment of Microbiology and Immunology, College of Medicine, University of Louisville, Louisville, KY, USA; Center for Predictive Medicine, College of Medicine, University of Louisville, Louisville, KY, USA. Electronic address: abukwaik@louisville.edu.
University of Louisville · USUniversity of Rijeka · HR

Funding

Understanding the Host-Microbiome-Therapeutic Triad: Implications for Designing Alternative IntravaginalP20GM125504 · NIGMS · UNIVERSITY OF LOUISVILLE · PI Shirin Ghods · 2018 to 2026
$24.4M
Innate immunity and inflammatory response of macrophages to Legionella infectionR01AI140195 · NIAID · UNIVERSITY OF LOUISVILLE · PI ABU KWAIK, YOUSEF A · 2018 to 2022
$1.9M
NIAID NIH HHS R01 AI140195NIGMS NIH HHS P20 GM125504
6 · The paper itself

Abstract

Legionella pneumophila has co-evolved with amoebae, their natural hosts. Upon transmission to humans, the bacteria proliferate within alveolar macrophages causing pneumonia. Here, we show L. pneumophila injects the effector LamA, an amylase, into the cytosol of human macrophage (hMDMs) and amoebae to rapidly degrade glycogen to generate cytosolic hyper-glucose. In response, hMDMs shift their metabolism to aerobic glycolysis, which directly triggers an M1-like pro-inflammatory differentiation and nutritional innate immunity through enhanced tryptophan degradation. This leads to a modest restriction of bacterial proliferation in hMDMs. In contrast, LamA-mediated glycogenolysis in amoebae deprives the natural host from the main building blocks for synthesis of the cellulose-rich cyst wall, leading to subversion of amoeba encystation. This is non-permissive for bacterial proliferation. Therefore, LamA of L. pneumophila is an amoebae host-adapted effector that subverts encystation of the amoebae natural host, and the paradoxical hMDMs' pro-inflammatory response is likely an evolutionary accident.

Indexed as

Legionella pneumophilaAmoebaAmylasesBiological EvolutionCytokinesGlycogenolysisHost-Parasite InteractionsHumansImmunity, InnateMacrophages, AlveolarParasite EncystmentAmylasesCytokinesamoebaeamylaseDot/IcmglycogenglycogenolysislegionellaM1macrophagepro-inflammatory

Identifiers

PMID32220647
PMCPMC7224327
OpenAlexW3013848808

What OpenQuestion holds

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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.