Evidence map›Paper›PMID 28752080›Full record

ReviewFrontiers in cellular and infection microbiology2017

To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection.

Wolfgang Eisenreich, Thomas Rudel, Jürgen Heesemann, Werner Goebel

Abstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Glyceraldehyde-3-phosphate dehydrogenase homologs as bifunctional gatekeepers of metabolic segregation inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Neutrophils: emerging perspectives on the pathogenesis of oral mucosal diseases.Frontiers in cellular and infection microbiology · 2025
    Review
  7. Article
  8. Metabolism and physiology of pathogenic bacterial obligate intracellular parasites.Frontiers in cellular and infection microbiology · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Uncovering the Hidden Credentials ofMicrobiology and molecular biology reviews : MMBR · 2021
    Review
  15. Review
  16. Article
  17. Article
  18. FX11 limitsDisease models & mechanisms · 2020
    Article
  19. Review
  20. Microbiology spectrum · 2019
    Review
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

4 authors.

Wolfgang EisenreichDepartment of Chemistry, Chair of Biochemistry, Technische Universität MünchenGarching, Germany.
Thomas RudelDepartment of Microbiology, Biocenter, University of WürzburgWürzburg, Germany.
Jürgen HeesemannMax von Pettenkofer-Institute, Chair of Medical Microbiology and Hospital Epidemiology, Ludwig Maximilian University of MunichMünchen, Germany.
Werner GoebelMax von Pettenkofer-Institute, Chair of Medical Microbiology and Hospital Epidemiology, Ludwig Maximilian University of MunichMünchen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular bacterial pathogens (IBPs) invade and replicate in different cell types including immune cells, in particular of the innate immune system (IIS) during infection in the acute phase. However, immune cells primarily function as essential players in the highly effective and integrated host defense systems comprising the IIS and the adaptive immune system (AIS), which cooperatively protect the host against invading microbes including IBPs. As countermeasures, the bacterial pathogens (and in particular the IBPs) have developed strategies to evade or reprogram the IIS at various steps. The intracellular replication capacity and the anti-immune defense responses of the IBP's as well as the specific antimicrobial responses of the immune cells of the innate and the AIS depend on specific metabolic programs of the IBPs and their host cells. The metabolic programs of the immune cells supporting or counteracting replication of the IBPs appear to be mutually exclusive. Indeed, recent studies show that upon interaction of naïve, metabolically quiescent immune cells with IBPs, different metabolic activation processes occur which may result in the provision of a survival and replication niche for the pathogen or its eradication. It is therefore likely that within a possible host cell population subsets exist that are metabolically programmed for pro- or anti-microbial conditions. These metabolic programs may be triggered by the interactions between different bacterial agonistic components and host cell receptors. In this review, we summarize the current status in the field and discuss metabolic adaptation processes within immune cells of the IIS and the IBPs that support or restrict the intracellular replication of the pathogens.

Indexed as

AnimalsBacteriaBacterial InfectionsBlood CellsHost-Pathogen InteractionsHumansImmunity, Innateimmunometabolisminnate immune systemintracellular pathogensmetabolic adaptationpathometabolism

Identifiers

PMID28752080
PMCPMC5508010

What Socratic holds

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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 Socratic graph.