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.
Adipose Tissue
/ metabolism
Adolescent
Adult
Animals
Asthma
/ etiology
Causality
Child
DNA Methylation
Female
Gene Expression Regulation
Humans
Inflammation
Interleukin-17
/ genetics
Interleukin-23
/ physiology
Macrophages
/ metabolism
Male
Meta-Analysis as Topic
Mice
Middle Aged
Models, Immunological
Nuclear Receptor Subfamily 1, Group F, Member 3
/ genetics
Obesity
/ complications
Promoter Regions, Genetic
Th17 Cells
/ metabolism
Tumor Necrosis Factor-alpha
/ genetics
IL-17A
Methylation
Non-atopic asthma
Obesity
RORC
Tumour necrosis factor-alpha
Journal
Medical hypotheses
ISSN: 1532-2777
Titre abrégé: Med Hypotheses
Pays: United States
ID NLM: 7505668
Informations de publication
Date de publication:
Jan 2020
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
109527Commentaires et corrections
Type : ErratumIn
Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.