Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Detalhes bibliográficos
Autor(a) principal: Muc, Magdalena
Data de Publicação: 2016
Outros Autores: Mota-Pinto, Anabela, Padez, Cristina
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
Texto Completo: http://hdl.handle.net/10316/31909
https://doi.org/10.1017/S0954422416000111
Resumo: Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.
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spelling Association between obesity and asthma – epidemiology, pathophysiology and clinical profileObesidade/ObesityExcesso de peso/OverweightAsma/AsthmaFenótipos/PhenotypesAsma induzida por obesidade/Obesity-induced asthmaObesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.2016info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://hdl.handle.net/10316/31909http://hdl.handle.net/10316/31909https://doi.org/10.1017/S0954422416000111engMuc, MagdalenaMota-Pinto, AnabelaPadez, Cristinainfo:eu-repo/semantics/openAccessreponame:Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)instname:Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãoinstacron:RCAAP2022-05-25T06:47:27Zoai:estudogeral.uc.pt:10316/31909Portal AgregadorONGhttps://www.rcaap.pt/oai/openaireopendoar:71602024-03-19T20:43:40.839988Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos) - Agência para a Sociedade do Conhecimento (UMIC) - FCT - Sociedade da Informaçãofalse
dc.title.none.fl_str_mv Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
title Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
spellingShingle Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
Muc, Magdalena
Obesidade/Obesity
Excesso de peso/Overweight
Asma/Asthma
Fenótipos/Phenotypes
Asma induzida por obesidade/Obesity-induced asthma
title_short Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
title_full Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
title_fullStr Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
title_full_unstemmed Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
title_sort Association between obesity and asthma – epidemiology, pathophysiology and clinical profile
author Muc, Magdalena
author_facet Muc, Magdalena
Mota-Pinto, Anabela
Padez, Cristina
author_role author
author2 Mota-Pinto, Anabela
Padez, Cristina
author2_role author
author
dc.contributor.author.fl_str_mv Muc, Magdalena
Mota-Pinto, Anabela
Padez, Cristina
dc.subject.por.fl_str_mv Obesidade/Obesity
Excesso de peso/Overweight
Asma/Asthma
Fenótipos/Phenotypes
Asma induzida por obesidade/Obesity-induced asthma
topic Obesidade/Obesity
Excesso de peso/Overweight
Asma/Asthma
Fenótipos/Phenotypes
Asma induzida por obesidade/Obesity-induced asthma
description Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.
publishDate 2016
dc.date.none.fl_str_mv 2016
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
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dc.identifier.uri.fl_str_mv http://hdl.handle.net/10316/31909
http://hdl.handle.net/10316/31909
https://doi.org/10.1017/S0954422416000111
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https://doi.org/10.1017/S0954422416000111
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