Evidence map›Paper›PMID 38629728›Full record

ArticleImmunity, inflammation and disease2024

Adipose tissue IL-18 production is independent of caspase-1 and caspase-11.

Luis Román-Domínguez, Jonathan Salazar-León, Karla F Meza-Sosa, Leonor Pérez-Martínez, Gustavo Pedraza-Alva

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Luis Román-DomínguezLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.
Jonathan Salazar-LeónLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.
Karla F Meza-SosaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.ORCID 0000-0002-0095-2357
Leonor Pérez-MartínezLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.ORCID 0000-0003-4163-1653
Gustavo Pedraza-AlvaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.ORCID 0000-0002-6978-1218
Universidad Nacional Autónoma de México · MX

Funding

Consejo Nacional de Ciencia y Tecnología CF-2019/40792Consejo Nacional de Ciencia y Tecnología IFC-2016/2282Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN211719Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN213119Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN216922Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México IN217822
6 · The paper itself

Abstract

backgroundInflammation in adipose tissue, resulting from imbalanced caloric intake and energy expenditure, contributes to the metabolic dysregulation observed in obesity. The production of inflammatory cytokines, such as IL-1β and IL-18, plays a key role in this process. While IL-1β promotes insulin resistance and diabetes, IL-18 regulates energy expenditure and food intake. Previous studies have suggested that caspase-1, activated by the Nlrp3 inflammasome in response to lipid excess, mediates IL-1β production, whereas activated by the Nlrp1b inflammasome in response to energy excess, mediates IL-18 production. However, this has not been formally tested.

methodsWild-type and caspase-1-deficient Balb/c mice, carrying the Nlrp1b1 allele, were fed with regular chow or a high-fat diet for twelve weeks. Food intake and mass gain were recorded weekly. At the end of the twelve weeks, glucose tolerance and insulin resistance were evaluated. Mature IL-18 protein levels and the inflammatory process in the adipose tissue were determined. Fasting lipid and cytokine levels were quantified in the sera of the different experimental groups.

resultsWe found that IL-18 production in adipose tissue is independent of caspase-1 activity, regardless of the metabolic state, while Nlrp3-mediated IL-1β production remains caspase-1 dependent. Additionally, caspase-1 null Balb/c mice did not develop metabolic abnormalities in response to energy excess from the high-fat diet.

conclusionOur findings suggest that IL-18 production in the adipose tissue is independent of Nlrp3 inflammasome and caspase-1 activation, regardless of caloric food intake. In contrast, Nlrp3-mediated IL-1β production is caspase-1 dependent. These results provide new insights into the mechanisms underlying cytokine production in the adipose tissue during both homeostatic conditions and metabolic stress, highlighting the distinct roles of caspase-1 and the Nlrp inflammasomes in regulating inflammatory responses.

Indexed as

Adipose TissueCaspase 1Caspases, InitiatorInterleukin-18NLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCaspasesCytokinesInflammasomesInsulin ResistanceLipidsMiceCasp4 protein, mouseCaspase 1CaspasesCaspases, InitiatorCytokinesInflammasomesInterleukin-18LipidsNLR Family, Pyrin Domain-Containing 3 Proteinadipose tissueanimalscytokinesdiabetesinflammationmacrophagemolecules

Identifiers

PMID38629728
PMCPMC11022623
OpenAlexW4394873322

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.