Alicia Martinek,Andrea Deinzer,Roman G Gerlach,Jana Petzold,Lea Semmler,Christof Vorsatz,Padraic G Fallon,Christian Schwartz
{"title":"肥胖损害皮肤屏障功能,促进小鼠过敏致敏。","authors":"Alicia Martinek,Andrea Deinzer,Roman G Gerlach,Jana Petzold,Lea Semmler,Christof Vorsatz,Padraic G Fallon,Christian Schwartz","doi":"10.1111/all.70067","DOIUrl":null,"url":null,"abstract":"Atopic dermatitis is a chronic inflammatory skin condition marked by intense itching and a weakened skin barrier. The compromised skin barrier often leads to exaggerated immune responses and greater sensitivity to allergens. Previous studies have already implicated a link between obesity and atopic dermatitis; however, the mechanisms linking obesity to atopy are not yet well understood. We propose that obesity impairs skin barrier function, facilitating allergen penetration in the skin and triggering systemic and local allergic sensitization. We used a diet-induced obesity mouse model to examine skin barrier integrity and immune responses in both steady-state and inflammatory conditions. In order to induce dermatitis or food allergy, we epicutaneously applied MC903 or ovalbumin, respectively. We observed that obesity significantly alters skin barrier physiology, as indicated by increased transepidermal water loss in obese animals. Over time, we observed a decrease in key skin barrier proteins-preceding overt cutaneous inflammation, further indicating a loss of barrier integrity during obesity. Interestingly, skin barrier breakdown was independent of changes to the microbiome. On a cellular level, immune profiling revealed a shift towards a type 17 helper T-cell response bias, although this shift did not coincide with an increase in cytokine production under steady-state conditions. Topical application of MC903 in obese animals led to increased ear swelling and a pronounced Th17-biased inflammatory response compared to lean counterparts. Our findings show that obesity weakens the skin barrier, facilitating increased allergen penetration and allergic sensitization. The Th17-skewed immune environment in obese animals may also amplify inflammatory responses to allergens and act as a feed-forward loop to further disintegrate the skin barrier. This study highlights how obesity-induced skin barrier dysfunction contributes to allergic conditions like atopic dermatitis and may be therapeutically targeted by barrier restoration.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"88 1","pages":""},"PeriodicalIF":12.0000,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Obesity Impairs Skin Barrier Function and Facilitates Allergic Sensitization in Mice.\",\"authors\":\"Alicia Martinek,Andrea Deinzer,Roman G Gerlach,Jana Petzold,Lea Semmler,Christof Vorsatz,Padraic G Fallon,Christian Schwartz\",\"doi\":\"10.1111/all.70067\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Atopic dermatitis is a chronic inflammatory skin condition marked by intense itching and a weakened skin barrier. The compromised skin barrier often leads to exaggerated immune responses and greater sensitivity to allergens. Previous studies have already implicated a link between obesity and atopic dermatitis; however, the mechanisms linking obesity to atopy are not yet well understood. We propose that obesity impairs skin barrier function, facilitating allergen penetration in the skin and triggering systemic and local allergic sensitization. We used a diet-induced obesity mouse model to examine skin barrier integrity and immune responses in both steady-state and inflammatory conditions. In order to induce dermatitis or food allergy, we epicutaneously applied MC903 or ovalbumin, respectively. We observed that obesity significantly alters skin barrier physiology, as indicated by increased transepidermal water loss in obese animals. Over time, we observed a decrease in key skin barrier proteins-preceding overt cutaneous inflammation, further indicating a loss of barrier integrity during obesity. Interestingly, skin barrier breakdown was independent of changes to the microbiome. On a cellular level, immune profiling revealed a shift towards a type 17 helper T-cell response bias, although this shift did not coincide with an increase in cytokine production under steady-state conditions. Topical application of MC903 in obese animals led to increased ear swelling and a pronounced Th17-biased inflammatory response compared to lean counterparts. Our findings show that obesity weakens the skin barrier, facilitating increased allergen penetration and allergic sensitization. The Th17-skewed immune environment in obese animals may also amplify inflammatory responses to allergens and act as a feed-forward loop to further disintegrate the skin barrier. This study highlights how obesity-induced skin barrier dysfunction contributes to allergic conditions like atopic dermatitis and may be therapeutically targeted by barrier restoration.\",\"PeriodicalId\":122,\"journal\":{\"name\":\"Allergy\",\"volume\":\"88 1\",\"pages\":\"\"},\"PeriodicalIF\":12.0000,\"publicationDate\":\"2025-09-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Allergy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/all.70067\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Allergy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/all.70067","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ALLERGY","Score":null,"Total":0}
Obesity Impairs Skin Barrier Function and Facilitates Allergic Sensitization in Mice.
Atopic dermatitis is a chronic inflammatory skin condition marked by intense itching and a weakened skin barrier. The compromised skin barrier often leads to exaggerated immune responses and greater sensitivity to allergens. Previous studies have already implicated a link between obesity and atopic dermatitis; however, the mechanisms linking obesity to atopy are not yet well understood. We propose that obesity impairs skin barrier function, facilitating allergen penetration in the skin and triggering systemic and local allergic sensitization. We used a diet-induced obesity mouse model to examine skin barrier integrity and immune responses in both steady-state and inflammatory conditions. In order to induce dermatitis or food allergy, we epicutaneously applied MC903 or ovalbumin, respectively. We observed that obesity significantly alters skin barrier physiology, as indicated by increased transepidermal water loss in obese animals. Over time, we observed a decrease in key skin barrier proteins-preceding overt cutaneous inflammation, further indicating a loss of barrier integrity during obesity. Interestingly, skin barrier breakdown was independent of changes to the microbiome. On a cellular level, immune profiling revealed a shift towards a type 17 helper T-cell response bias, although this shift did not coincide with an increase in cytokine production under steady-state conditions. Topical application of MC903 in obese animals led to increased ear swelling and a pronounced Th17-biased inflammatory response compared to lean counterparts. Our findings show that obesity weakens the skin barrier, facilitating increased allergen penetration and allergic sensitization. The Th17-skewed immune environment in obese animals may also amplify inflammatory responses to allergens and act as a feed-forward loop to further disintegrate the skin barrier. This study highlights how obesity-induced skin barrier dysfunction contributes to allergic conditions like atopic dermatitis and may be therapeutically targeted by barrier restoration.
期刊介绍:
Allergy is an international and multidisciplinary journal that aims to advance, impact, and communicate all aspects of the discipline of Allergy/Immunology. It publishes original articles, reviews, position papers, guidelines, editorials, news and commentaries, letters to the editors, and correspondences. The journal accepts articles based on their scientific merit and quality.
Allergy seeks to maintain contact between basic and clinical Allergy/Immunology and encourages contributions from contributors and readers from all countries. In addition to its publication, Allergy also provides abstracting and indexing information. Some of the databases that include Allergy abstracts are Abstracts on Hygiene & Communicable Disease, Academic Search Alumni Edition, AgBiotech News & Information, AGRICOLA Database, Biological Abstracts, PubMed Dietary Supplement Subset, and Global Health, among others.