Evidence map›Paper›PMID 37101405›Full record

ArticleAging cell2023

Metabololipidomic and proteomic profiling reveals aberrant macrophage activation and interrelated immunomodulatory mediator release during aging.

Patrick Schädel, Anna Czapka, Nadja Gebert, Ilse Denise Jacobsen, Alessandro Ori, Oliver Werz

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
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

13 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Sex hormone deprivation abolishes sex-specific differences in murine colon inflammation and related lipid mediator production.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. 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

6 authors at 3 institutions in 1 country.

Patrick SchädelDepartment of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich-Schiller University, Jena, Germany.ORCID 0000-0002-9586-6653
Anna CzapkaDepartment of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich-Schiller University, Jena, Germany.ORCID 0000-0002-6849-7020
Nadja GebertLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.ORCID 0000-0002-7659-3426
Ilse Denise JacobsenLeibniz Institute for Natural Product Research and Infection Biology - Hans Knoell Institute (HKI), Jena, Germany.ORCID 0000-0002-6033-9984
Alessandro OriLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.ORCID 0000-0002-3046-0871
Oliver WerzDepartment of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, Friedrich-Schiller University, Jena, Germany.ORCID 0000-0002-5064-4379
Friedrich Schiller University Jena · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages adapt distinct pro-inflammatory (M1-like) and pro-resolving (M2-like) phenotypes with specific tasks in the immune response and tissue homeostasis. Altered macrophage responses with age are causative for unresolved inflammation, so-called inflammaging, and lead to higher infection susceptibility with unfavorable progression. Here, we reveal molecular determinants of age-related changes in phenotypic functions of murine peritoneal macrophages (PM) by employing comprehensive mass spectrometry-based proteomics (4746 protein groups) and metabololipidomics (>40 lipid mediators). Divergent expression of various macrophage-specific marker proteins and signaling pathways indicates aberrant PM phenotypes in old mice which detrimentally impact their capabilities to release immunomodulatory chemokines and cytokines. We show that aging strikingly compromises the polarization process of macrophages to adapt either pro-inflammatory or pro-resolving phenotypes, thereby yielding aberrant and afunctional macrophage subtypes that cannot be readily assigned to either a typical M1 or M2 phenotype. In particular, the phenotypic adaptation of the bacteria-challenged metabololipidome in macrophages related to inflammation is severely limited by age, which persists across ex vivo polarization towards M1 and M2a macrophages. Our results establish distinct age-associated PM phenotypes outside of the simplified M1 and M2 dichotomy and challenge the dogma of increased pro-inflammatory macrophage pre-activation due to aging by revealing maladaptive functions throughout all phases of inflammation, including resolution.

Indexed as

Macrophage ActivationProteomicsAgingAnimalsImmunityInflammationMiceagingeicosanoidsinflammationlipidomicsmacrophage activationmediators of inflammationperitoneal macrophagesproteomics

Identifiers

PMID37101405
PMCPMC10352559
OpenAlexW4367174663

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.