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Regulation of eotaxin expression in skin allergic diseases

INTRODUCTION: As a key chemotactic factor during Eos recruitment on the allergic inflammation site, eotaxin is regarded as one of the important therapeutic targets. AIM: To address the expression and regulation mechanism of eotaxin, which constitutes an important procedure in skin allergic disease a...

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Autores principales: Peng, Cheng, Zhang, Hualin, Yang, Jishun, Xu, Jianguo, Guan, Shikui, Xia, Jianjun, Zhu, Quangang, You, Benming, Zhu, Yu, Hu, Jinhong, Liu, Jiyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326924/
https://www.ncbi.nlm.nih.gov/pubmed/35950112
http://dx.doi.org/10.5114/ada.2022.117739
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author Peng, Cheng
Zhang, Hualin
Yang, Jishun
Xu, Jianguo
Guan, Shikui
Xia, Jianjun
Zhu, Quangang
You, Benming
Zhu, Yu
Hu, Jinhong
Liu, Jiyong
author_facet Peng, Cheng
Zhang, Hualin
Yang, Jishun
Xu, Jianguo
Guan, Shikui
Xia, Jianjun
Zhu, Quangang
You, Benming
Zhu, Yu
Hu, Jinhong
Liu, Jiyong
author_sort Peng, Cheng
collection PubMed
description INTRODUCTION: As a key chemotactic factor during Eos recruitment on the allergic inflammation site, eotaxin is regarded as one of the important therapeutic targets. AIM: To address the expression and regulation mechanism of eotaxin, which constitutes an important procedure in skin allergic disease and a target for drug therapy. MATERIAL AND METHODS: An allergic contact dermatitis (ACD) model of mouse was established. Immunohistochemical method (ICH) and flow cytometry method (FCM) were used to determine the amounts of CD4+ and CD8+ T cells and their ratios. The eotaxin mRNA and protein were evaluated by real-time PCR, ICH and western-blotting method. Nuclear factor-κB (NF-κB) nuclear translocation and STAT6 phosphorylation were studied by EMSA and western-blotting methods. RESULTS: We confirmed that both CD4+ and CD8+ T cells in mouse blood and tissue increased during the allergic process, FBs was the main source for eotaxin under the allergic condition. Both TNF-α and IL-4 showed synergic effects on the up-regulation of eotaxin mRNA and protein in KC and FBs. Eotaxin can be expressed via NF-κB and STAT6 transcription after KC and FBs were stimulated by TNF-α and IL-4. CONCLUSIONS: The obvious up-regulation of eotaxin expression in skin tissue of the mouse ACD model was confirmed, the exact expression site and dynamic process was determined both in vivo and in vitro. The eotaxin expression ability of FBs outperformed that of KC, and eotaxin expression can be regulated by TNF-α and IL-4 via NF-κB and STAT6. The overall findings may pave the way for discovering targets for new drugs and new therapeutic drugs for treating allergic diseases.
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spelling pubmed-93269242022-08-09 Regulation of eotaxin expression in skin allergic diseases Peng, Cheng Zhang, Hualin Yang, Jishun Xu, Jianguo Guan, Shikui Xia, Jianjun Zhu, Quangang You, Benming Zhu, Yu Hu, Jinhong Liu, Jiyong Postepy Dermatol Alergol Original Paper INTRODUCTION: As a key chemotactic factor during Eos recruitment on the allergic inflammation site, eotaxin is regarded as one of the important therapeutic targets. AIM: To address the expression and regulation mechanism of eotaxin, which constitutes an important procedure in skin allergic disease and a target for drug therapy. MATERIAL AND METHODS: An allergic contact dermatitis (ACD) model of mouse was established. Immunohistochemical method (ICH) and flow cytometry method (FCM) were used to determine the amounts of CD4+ and CD8+ T cells and their ratios. The eotaxin mRNA and protein were evaluated by real-time PCR, ICH and western-blotting method. Nuclear factor-κB (NF-κB) nuclear translocation and STAT6 phosphorylation were studied by EMSA and western-blotting methods. RESULTS: We confirmed that both CD4+ and CD8+ T cells in mouse blood and tissue increased during the allergic process, FBs was the main source for eotaxin under the allergic condition. Both TNF-α and IL-4 showed synergic effects on the up-regulation of eotaxin mRNA and protein in KC and FBs. Eotaxin can be expressed via NF-κB and STAT6 transcription after KC and FBs were stimulated by TNF-α and IL-4. CONCLUSIONS: The obvious up-regulation of eotaxin expression in skin tissue of the mouse ACD model was confirmed, the exact expression site and dynamic process was determined both in vivo and in vitro. The eotaxin expression ability of FBs outperformed that of KC, and eotaxin expression can be regulated by TNF-α and IL-4 via NF-κB and STAT6. The overall findings may pave the way for discovering targets for new drugs and new therapeutic drugs for treating allergic diseases. Termedia Publishing House 2022-07-14 2022-06 /pmc/articles/PMC9326924/ /pubmed/35950112 http://dx.doi.org/10.5114/ada.2022.117739 Text en Copyright: © 2022 Termedia Sp. z o. o. https://creativecommons.org/licenses/by-nc-sa/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
spellingShingle Original Paper
Peng, Cheng
Zhang, Hualin
Yang, Jishun
Xu, Jianguo
Guan, Shikui
Xia, Jianjun
Zhu, Quangang
You, Benming
Zhu, Yu
Hu, Jinhong
Liu, Jiyong
Regulation of eotaxin expression in skin allergic diseases
title Regulation of eotaxin expression in skin allergic diseases
title_full Regulation of eotaxin expression in skin allergic diseases
title_fullStr Regulation of eotaxin expression in skin allergic diseases
title_full_unstemmed Regulation of eotaxin expression in skin allergic diseases
title_short Regulation of eotaxin expression in skin allergic diseases
title_sort regulation of eotaxin expression in skin allergic diseases
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9326924/
https://www.ncbi.nlm.nih.gov/pubmed/35950112
http://dx.doi.org/10.5114/ada.2022.117739
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