Evidence map›Paper›PMID 28384279›Full record

ArticlePLoS pathogens2017

Host cell-derived lactate functions as an effector molecule in Neisseria meningitidis microcolony dispersal.

Sara Sigurlásdóttir, Jakob Engman, Olaspers Sara Eriksson, Sunil D Saroj, Nadezda Zguna, Pilar Lloris-Garcerá, Leopold L Ilag, Ann-Beth Jonsson

Abstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Internalization ofMicroorganisms · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022
    Review
  10. Review
  11. Lactate-Induced Dispersal ofInfection and immunity · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Deletion of D-Lactate Dehydrogenase A inFrontiers in microbiology · 2019
    Article
  17. Article
  18. Quantification ofBio-protocol · 2018
    Article
  19. Live-cell Imaging ofBio-protocol · 2018
    Article
  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

8 authors.

Sara SigurlásdóttirDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Jakob EngmanDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Olaspers Sara ErikssonDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Sunil D SarojDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
Nadezda ZgunaDepartment of Environmental Science and Analytical Chemistry, Stockholm University, Stockholm, Sweden.
Pilar Lloris-GarceráDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-2487-9860
Leopold L IlagDepartment of Environmental Science and Analytical Chemistry, Stockholm University, Stockholm, Sweden.
Ann-Beth JonssonDepartment of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4480-2940

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of meningococcal disease, caused by the human pathogen Neisseria meningitidis, is preceded by the colonization of the epithelial layer in the nasopharynx. After initial adhesion to host cells meningococci form aggregates, through pilus-pilus interactions, termed microcolonies from which the bacteria later detach. Dispersal from microcolonies enables access to new colonization sites and facilitates the crossing of the cell barrier; however, this process is poorly understood. In this study, we used live-cell imaging to investigate the process of N. meningitidis microcolony dispersal. We show that direct contact with host cells is not required for microcolony dispersal, instead accumulation of a host-derived effector molecule induces microcolony dispersal. By using a host-cell free approach, we demonstrated that lactate, secreted from host cells, initiate rapid dispersal of microcolonies. Interestingly, metabolic utilization of lactate by the bacteria was not required for induction of dispersal, suggesting that lactate plays a role as a signaling molecule. Furthermore, Neisseria gonorrhoeae microcolony dispersal could also be induced by lactate. These findings reveal a role of host-secreted lactate in microcolony dispersal and virulence of pathogenic Neisseria.

Indexed as

Bacterial AdhesionBacterial ProteinsEpithelial CellsFimbriae, BacterialHumansLactic AcidMeningococcal InfectionsNeisseria gonorrhoeaeNeisseria meningitidisVirulenceBacterial ProteinsLactic Acid

Identifiers

PMID28384279
PMCPMC5383330

What OpenQuestion holds

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Registered trials

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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.