A novel mouse model of atopic dermatitis with epicutaneous allergen sensitization and the effect of Lactobacillus rhamnosus
Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model base...
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Published in | Experimental dermatology Vol. 21; no. 9; pp. 672 - 675 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Blackwell Publishing Ltd
01.09.2012
Blackwell |
Subjects | |
Online Access | Get full text |
ISSN | 0906-6705 1600-0625 1600-0625 |
DOI | 10.1111/j.1600-0625.2012.01539.x |
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Abstract | Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside–inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH‐1 hairless mice underwent three 1‐week exposures (separated by 2‐week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 109 CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA‐specific IgE and skin expression of interleukin‐4 (IL‐4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+ Foxp3+ Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the ‘outside–inside’ theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL‐4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells. |
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AbstractList | Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9) CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells. Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 109CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+Foxp3+Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells. Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9) CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells.Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside-inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH-1 hairless mice underwent three 1-week exposures (separated by 2-week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 10(9) CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA-specific IgE and skin expression of interleukin-4 (IL-4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4(+) CD25(+) Foxp3(+) Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the 'outside-inside' theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL-4 and TSLP in the skin via a mechanism that may involve CD4(+) CD25(+) Foxp3(+) Treg cells. Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse models of AD, it is not easy to establish model to represent the natural AD development in human. In this study, we developed an AD model based on outside–inside theory and investigated the effect of Lactobacillus rhamnosus (Lcr35), which have known as an immune modulator in allergic diseases. SKH‐1 hairless mice underwent three 1‐week exposures (separated by 2‐week intervals) to an ovalbumin (OVA) or saline (control) patch at the same site to develop the mouse model of AD. Lcr35 (1 × 109 CFU) was administered orally every day from 1 week before the first sensitization until the end of the study. The AD model induced erythematous and itchy skin, increasing TEWL and increasing skin inflammation as assessed by histology in the mice. Oral Lcr35 attenuated all disease parameters previously mentioned. OVA‐specific IgE and skin expression of interleukin‐4 (IL‐4) and thymic stromal lymphopoietin (TSLP) increased in AD mice, but were reduced in AD mice treated with Lcr35. Moreover, Lcr35 treatment led to an increase in CD4+CD25+ Foxp3+ Treg cells in the mesenteric lymph nodes of AD mice. In conclusions, based on the ‘outside–inside’ theory, topical allergen may induce AD without skin injury. Oral application of Lcr35 prevented the development of AD in this model by suppressing production of the inflammatory cytokines, IL‐4 and TSLP in the skin via a mechanism that may involve CD4+CD25+Foxp3+Treg cells. |
Author | Lee, Seung-Hun Seo, Ju-Hee Kim, Ji-Min Kang, Mi-Jin Kim, Young-Joon Kim, Ha-Jung Kim, Hyung-Young Jeong, Se Kyoo Hong, Soo-Jong |
Author_xml | – sequence: 1 givenname: Ha-Jung surname: Kim fullname: Kim, Ha-Jung organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea – sequence: 2 givenname: Young-Joon surname: Kim fullname: Kim, Young-Joon organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea – sequence: 3 givenname: Mi-Jin surname: Kang fullname: Kang, Mi-Jin organization: Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea – sequence: 4 givenname: Ju-Hee surname: Seo fullname: Seo, Ju-Hee organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea – sequence: 5 givenname: Hyung-Young surname: Kim fullname: Kim, Hyung-Young organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea – sequence: 6 givenname: Se Kyoo surname: Jeong fullname: Jeong, Se Kyoo organization: Applied Research Division, NeoPharm Co., Ltd., Daejeon, Korea – sequence: 7 givenname: Seung-Hun surname: Lee fullname: Lee, Seung-Hun organization: Department of Dermatology, Human Barrier Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea – sequence: 8 givenname: Ji-Min surname: Kim fullname: Kim, Ji-Min organization: Department of Dermatology, Human Barrier Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea – sequence: 9 givenname: Soo-Jong surname: Hong fullname: Hong, Soo-Jong email: sjhong@amc.seoul.kr organization: Department of Pediatrics, Childhood Asthma Atopy Center, Research Center for Standardization of Allergic Diseases, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea |
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Keywords | Probiotic Immunopathology Allergy Skin disease Thymus gland Dermatology Rodentia regulatory mice Atopy Vertebrata T-lymphocytes thymic stromal lymphopoietin Mammalia Mouse Atopic dermatitis Animal T-Lymphocyte Bacteria Lactobacillaceae Models Sensitization Lactobacillus rhamnosus probiotics |
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Snippet | Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease, and the pathogenesis is not completely understood. Although there are some mouse... |
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SubjectTerms | Allergens Allergic diseases Analysis of Variance Animal models Animals Atopic dermatitis Biological and medical sciences CD4 Antigens - metabolism Cytokines - metabolism Dermatitis, Atopic - immunology Dermatitis, Atopic - metabolism Dermatitis, Atopic - physiopathology Dermatology Disease Models, Animal Female Forkhead Transcription Factors - metabolism Hairless Immunoglobulin E Immunoglobulin E - blood Immunomodulation Immunopathology Inflammation Inflammatory diseases Injuries Interleukin 4 Interleukin-2 Receptor alpha Subunit - metabolism Interleukin-4 - metabolism Lactobacillus rhamnosus Lactobacillus rhamnosus - immunology Lymph nodes Lymph Nodes - immunology Lymphocyte Count Medical sciences Mesentery Mice Mice, Hairless Ovalbumin Ovalbumin - immunology Permeability - drug effects probiotics Probiotics - pharmacology regulatory Skin - metabolism Skin allergic diseases. Stinging insect allergies Skin diseases T-lymphocytes T-Lymphocytes, Regulatory - immunology T-Lymphocytes, Regulatory - metabolism Thymic stromal lymphopoietin Water - metabolism |
Title | A novel mouse model of atopic dermatitis with epicutaneous allergen sensitization and the effect of Lactobacillus rhamnosus |
URI | https://api.istex.fr/ark:/67375/WNG-KG2P1FQJ-G/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1600-0625.2012.01539.x https://www.ncbi.nlm.nih.gov/pubmed/22742655 https://www.proquest.com/docview/1034200329 https://www.proquest.com/docview/1038612779 |
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