Asthma, obesity, and microbiota: A complex immunological interaction
•Obesity increases the risk of asthma development and worsens the symptoms, affecting children and adults by different mechanisms.•The influence of obesity can start as early as in the womb by promoting epigenetic alterations, and by affecting the bacterial colonization of the offspring in a detrime...
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Veröffentlicht in: | Immunology letters 2023-03, Vol.255, p.10-20 |
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description | •Obesity increases the risk of asthma development and worsens the symptoms, affecting children and adults by different mechanisms.•The influence of obesity can start as early as in the womb by promoting epigenetic alterations, and by affecting the bacterial colonization of the offspring in a detrimental way.•High-fat diet and obesity promote gut dysbiosis, however, their influence over lung microbiota is still poorly assessed.
Obesity and allergic asthma are inflammatory chronic diseases mediated by distinct immunological features, obesity presents a Th1/Th17 profile, asthma is commonly associated with Th2 response. However, when combined, they result in more severe asthma symptoms, greater frequency of exacerbation episodes, and lower therapy responsiveness. These features lead to decreased life quality, associated with higher morbidity/mortality rates. In addition, obesity prompts specific asthma phenotypes, which can be dependent on atopic status, age, and gender. In adults, obesity is associated with neutrophilic/Th17 profile, while in children, the outcome is diverse, in some cases children with obesity present aggravation of atopy, and Th2 inflammation, and in others an association with a Th1 profile, with reduced IgE levels and eosinophilia. These alterations occur due to a complex group of factors among which the microbiome has been recently explored. Particularly, evidence shows its important role in susceptibility or resistance to asthma development, via gut-lung-axis, and demonstrates its relevance to the immune pathogenesis of the syndrome. Few studies address the relevance of the lung microbiome in shaping the immune response, locally. However, specific bacteria, like Moraxella catarrhalis, Haemophilus influenza, and Streptococcus pneumoniae, correlate with important features of the obese-asthmatic phenotype. Although maternal obesity is known to increase asthma risk in offspring, the impact on lung colonization is unknown. This review details the main key immune mechanisms involved in obesity-aggravated asthma, featuring the effect of maternal obesity in the establishment of gut and lung microbiota of the offspring, acting as potential childhood asthma inducer. |
doi_str_mv | 10.1016/j.imlet.2023.01.004 |
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Obesity and allergic asthma are inflammatory chronic diseases mediated by distinct immunological features, obesity presents a Th1/Th17 profile, asthma is commonly associated with Th2 response. However, when combined, they result in more severe asthma symptoms, greater frequency of exacerbation episodes, and lower therapy responsiveness. These features lead to decreased life quality, associated with higher morbidity/mortality rates. In addition, obesity prompts specific asthma phenotypes, which can be dependent on atopic status, age, and gender. In adults, obesity is associated with neutrophilic/Th17 profile, while in children, the outcome is diverse, in some cases children with obesity present aggravation of atopy, and Th2 inflammation, and in others an association with a Th1 profile, with reduced IgE levels and eosinophilia. These alterations occur due to a complex group of factors among which the microbiome has been recently explored. Particularly, evidence shows its important role in susceptibility or resistance to asthma development, via gut-lung-axis, and demonstrates its relevance to the immune pathogenesis of the syndrome. Few studies address the relevance of the lung microbiome in shaping the immune response, locally. However, specific bacteria, like Moraxella catarrhalis, Haemophilus influenza, and Streptococcus pneumoniae, correlate with important features of the obese-asthmatic phenotype. Although maternal obesity is known to increase asthma risk in offspring, the impact on lung colonization is unknown. This review details the main key immune mechanisms involved in obesity-aggravated asthma, featuring the effect of maternal obesity in the establishment of gut and lung microbiota of the offspring, acting as potential childhood asthma inducer.</description><identifier>ISSN: 0165-2478</identifier><identifier>EISSN: 1879-0542</identifier><identifier>DOI: 10.1016/j.imlet.2023.01.004</identifier><identifier>PMID: 36646290</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Asthma ; Female ; Humans ; Immune response ; Lung - pathology ; Maternal obesity ; Microbiota ; Obesity ; Obesity, Maternal - complications ; Obesity, Maternal - pathology ; Pregnancy</subject><ispartof>Immunology letters, 2023-03, Vol.255, p.10-20</ispartof><rights>2023 European Federation of Immunological Societies</rights><rights>Copyright © 2023 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c359t-ed833fc2bff13c4ba75c529c7a5daea2b67051be7d40ddff3b675b53471ccda3</citedby><cites>FETCH-LOGICAL-c359t-ed833fc2bff13c4ba75c529c7a5daea2b67051be7d40ddff3b675b53471ccda3</cites><orcidid>0000-0002-5294-8376 ; 0000-0001-9083-5834 ; 0000-0002-9740-564X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0165247823000044$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36646290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Menegati, Laura Machado</creatorcontrib><creatorcontrib>de Oliveira, Erick Esteves</creatorcontrib><creatorcontrib>Oliveira, Bernardo de Castro</creatorcontrib><creatorcontrib>Macedo, Gilson Costa</creatorcontrib><creatorcontrib>de Castro e Silva, Flávia Márcia</creatorcontrib><title>Asthma, obesity, and microbiota: A complex immunological interaction</title><title>Immunology letters</title><addtitle>Immunol Lett</addtitle><description>•Obesity increases the risk of asthma development and worsens the symptoms, affecting children and adults by different mechanisms.•The influence of obesity can start as early as in the womb by promoting epigenetic alterations, and by affecting the bacterial colonization of the offspring in a detrimental way.•High-fat diet and obesity promote gut dysbiosis, however, their influence over lung microbiota is still poorly assessed.
Obesity and allergic asthma are inflammatory chronic diseases mediated by distinct immunological features, obesity presents a Th1/Th17 profile, asthma is commonly associated with Th2 response. However, when combined, they result in more severe asthma symptoms, greater frequency of exacerbation episodes, and lower therapy responsiveness. These features lead to decreased life quality, associated with higher morbidity/mortality rates. In addition, obesity prompts specific asthma phenotypes, which can be dependent on atopic status, age, and gender. In adults, obesity is associated with neutrophilic/Th17 profile, while in children, the outcome is diverse, in some cases children with obesity present aggravation of atopy, and Th2 inflammation, and in others an association with a Th1 profile, with reduced IgE levels and eosinophilia. These alterations occur due to a complex group of factors among which the microbiome has been recently explored. Particularly, evidence shows its important role in susceptibility or resistance to asthma development, via gut-lung-axis, and demonstrates its relevance to the immune pathogenesis of the syndrome. Few studies address the relevance of the lung microbiome in shaping the immune response, locally. However, specific bacteria, like Moraxella catarrhalis, Haemophilus influenza, and Streptococcus pneumoniae, correlate with important features of the obese-asthmatic phenotype. Although maternal obesity is known to increase asthma risk in offspring, the impact on lung colonization is unknown. This review details the main key immune mechanisms involved in obesity-aggravated asthma, featuring the effect of maternal obesity in the establishment of gut and lung microbiota of the offspring, acting as potential childhood asthma inducer.</description><subject>Asthma</subject><subject>Female</subject><subject>Humans</subject><subject>Immune response</subject><subject>Lung - pathology</subject><subject>Maternal obesity</subject><subject>Microbiota</subject><subject>Obesity</subject><subject>Obesity, Maternal - complications</subject><subject>Obesity, Maternal - pathology</subject><subject>Pregnancy</subject><issn>0165-2478</issn><issn>1879-0542</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtOwzAQRS0EouXxBUgoSxZNGNtx0iKxqMpTQmLD3nLsCbiK4xK7iP49hhaWrEYanXncQ8gZhYICrS6XhXUdxoIB4wXQAqDcI2M6rWc5iJLtk3GiRM7KejoiRyEsAajgJT8kI15VZcVmMCY38xDfnJpkvsFg42aSqd5kzurBN9ZHdZXNM-3dqsPPzDq37n3nX61WXWb7iIPS0fr-hBy0qgt4uqvH5OXu9mXxkD893z8u5k-55mIWczRTzlvNmralXJeNqoUWbKZrJYxCxZqqBkEbrE0JxrQtTw3RpJdrqrVR_JhcbNeuBv--xhCls0Fj16ke_TpIVqdYHAB4QvkWTTlCGLCVq8E6NWwkBfltTy7ljz35bU8ClclemjrfHVg3Ds3fzK-uBFxvAUwpPywOMmiLvUZjB9RRGm__PfAFp4OCZw</recordid><startdate>202303</startdate><enddate>202303</enddate><creator>Menegati, Laura Machado</creator><creator>de Oliveira, Erick Esteves</creator><creator>Oliveira, Bernardo de Castro</creator><creator>Macedo, Gilson Costa</creator><creator>de Castro e Silva, Flávia Márcia</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5294-8376</orcidid><orcidid>https://orcid.org/0000-0001-9083-5834</orcidid><orcidid>https://orcid.org/0000-0002-9740-564X</orcidid></search><sort><creationdate>202303</creationdate><title>Asthma, obesity, and microbiota: A complex immunological interaction</title><author>Menegati, Laura Machado ; de Oliveira, Erick Esteves ; Oliveira, Bernardo de Castro ; Macedo, Gilson Costa ; de Castro e Silva, Flávia Márcia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-ed833fc2bff13c4ba75c529c7a5daea2b67051be7d40ddff3b675b53471ccda3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Asthma</topic><topic>Female</topic><topic>Humans</topic><topic>Immune response</topic><topic>Lung - pathology</topic><topic>Maternal obesity</topic><topic>Microbiota</topic><topic>Obesity</topic><topic>Obesity, Maternal - complications</topic><topic>Obesity, Maternal - pathology</topic><topic>Pregnancy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Menegati, Laura Machado</creatorcontrib><creatorcontrib>de Oliveira, Erick Esteves</creatorcontrib><creatorcontrib>Oliveira, Bernardo de Castro</creatorcontrib><creatorcontrib>Macedo, Gilson Costa</creatorcontrib><creatorcontrib>de Castro e Silva, Flávia Márcia</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Immunology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Menegati, Laura Machado</au><au>de Oliveira, Erick Esteves</au><au>Oliveira, Bernardo de Castro</au><au>Macedo, Gilson Costa</au><au>de Castro e Silva, Flávia Márcia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Asthma, obesity, and microbiota: A complex immunological interaction</atitle><jtitle>Immunology letters</jtitle><addtitle>Immunol Lett</addtitle><date>2023-03</date><risdate>2023</risdate><volume>255</volume><spage>10</spage><epage>20</epage><pages>10-20</pages><issn>0165-2478</issn><eissn>1879-0542</eissn><abstract>•Obesity increases the risk of asthma development and worsens the symptoms, affecting children and adults by different mechanisms.•The influence of obesity can start as early as in the womb by promoting epigenetic alterations, and by affecting the bacterial colonization of the offspring in a detrimental way.•High-fat diet and obesity promote gut dysbiosis, however, their influence over lung microbiota is still poorly assessed.
Obesity and allergic asthma are inflammatory chronic diseases mediated by distinct immunological features, obesity presents a Th1/Th17 profile, asthma is commonly associated with Th2 response. However, when combined, they result in more severe asthma symptoms, greater frequency of exacerbation episodes, and lower therapy responsiveness. These features lead to decreased life quality, associated with higher morbidity/mortality rates. In addition, obesity prompts specific asthma phenotypes, which can be dependent on atopic status, age, and gender. In adults, obesity is associated with neutrophilic/Th17 profile, while in children, the outcome is diverse, in some cases children with obesity present aggravation of atopy, and Th2 inflammation, and in others an association with a Th1 profile, with reduced IgE levels and eosinophilia. These alterations occur due to a complex group of factors among which the microbiome has been recently explored. Particularly, evidence shows its important role in susceptibility or resistance to asthma development, via gut-lung-axis, and demonstrates its relevance to the immune pathogenesis of the syndrome. Few studies address the relevance of the lung microbiome in shaping the immune response, locally. However, specific bacteria, like Moraxella catarrhalis, Haemophilus influenza, and Streptococcus pneumoniae, correlate with important features of the obese-asthmatic phenotype. Although maternal obesity is known to increase asthma risk in offspring, the impact on lung colonization is unknown. This review details the main key immune mechanisms involved in obesity-aggravated asthma, featuring the effect of maternal obesity in the establishment of gut and lung microbiota of the offspring, acting as potential childhood asthma inducer.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>36646290</pmid><doi>10.1016/j.imlet.2023.01.004</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5294-8376</orcidid><orcidid>https://orcid.org/0000-0001-9083-5834</orcidid><orcidid>https://orcid.org/0000-0002-9740-564X</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Asthma Female Humans Immune response Lung - pathology Maternal obesity Microbiota Obesity Obesity, Maternal - complications Obesity, Maternal - pathology Pregnancy |
title | Asthma, obesity, and microbiota: A complex immunological interaction |
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