Decreased methylation profiles in the TNFA gene promoters in type 1 macrophages and in the IL17A and RORC gene promoters in Th17 lymphocytes have a causal association with non-atopic asthma caused by obesity: A hypothesis.


Journal

Medical hypotheses
ISSN: 1532-2777
Titre abrégé: Med Hypotheses
Pays: United States
ID NLM: 7505668

Informations de publication

Date de publication:
Jan 2020
Historique:
received: 31 10 2019
accepted: 09 12 2019
pubmed: 27 12 2019
medline: 24 11 2020
entrez: 27 12 2019
Statut: ppublish

Résumé

Obesity is a serious public health problem worldwide and has been associated in epidemiological studies with a unique type of non-atopic asthma, although the causal association of asthma and obesity has certain criteria, such as the strength of association, consistency, specificity, temporality, biological gradient, coherence, analogy and experimentation; nevertheless, the biological plausibility of this association remains uncertain. Various mechanisms have been postulated, such as immunological, hormonal, mechanical, environmental, genetic and epigenetic mechanisms. Our hypothesis favours immunological mechanisms because some cytokines, such as tumour necrosis factor alpha (TNF-α) and interleukin (IL)-17A, are responsible for orchestrating low-grade systemic inflammation associated with obesity; however, these cytokines are regulated by epigenetic mechanisms, such as gene promoter methylation.

Identifiants

pubmed: 31877441
pii: S0306-9877(19)31035-7
doi: 10.1016/j.mehy.2019.109527
pii:
doi:

Substances chimiques

IL17A protein, human 0
Interleukin-17 0
Interleukin-23 0
Nuclear Receptor Subfamily 1, Group F, Member 3 0
RORC protein, human 0
Rorc protein, mouse 0
Tumor Necrosis Factor-alpha 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

109527

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

José J Leija-Martínez (JJ)

Universidad Nacional Autónoma de México, Mexico City, Mexico; Hospital Infantil de Mexico Federico Gómez, Research Laboratory of Pharmacology, Mexico City, Mexico.

Fengyang Huang (F)

Universidad Nacional Autónoma de México, Mexico City, Mexico; Hospital Infantil de Mexico Federico Gómez, Research Laboratory of Pharmacology, Mexico City, Mexico. Electronic address: huangfengyang@gmail.com.

Blanca E Del-Río-Navarro (BE)

Universidad Nacional Autónoma de México, Mexico City, Mexico; Hospital Infantil de México Federico Gómez, Department of Pediatric Allergy Clinical Immunology, Mexico City, Mexico.

Fausto Sanchéz-Muñoz (F)

Universidad Nacional Autónoma de México, Mexico City, Mexico; Departamento de Inmunología, Instituto Nacional de Cardiología "Ignacio Chávez", Mexico City, Mexico.

Rodrigo Romero-Nava (R)

Hospital Infantil de Mexico Federico Gómez, Research Laboratory of Pharmacology, Mexico City, Mexico; Laboratory of Pharmacology, Department of Health Sciences, Division of Health and Biological Sciences, Metropolitan Autonomous University of Iztapalapa, Mexico City, Mexico.

Onofre Muñoz-Hernandez (O)

Universidad Nacional Autónoma de México, Mexico City, Mexico.

Octavio Rodríguez-Cortés (O)

Laboratorio 103, SEPI, Escuela Superior de Medicina, Instituto Politécnico Nacional, Calle Plan de San Luis y Díaz Mirón S/N, Casco de Santo Tomas, Miguel Hidalgo, 11340 Ciudad de México, Mexico.

Margareth S Hall-Mondragon (MS)

Hospital Infantil de Mexico Federico Gómez, Research Laboratory of Pharmacology, Mexico City, Mexico.

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Classifications MeSH