Yue-Peng An, Rui Yuan, Shan-Shan Wang, Su-Qing Yang, Qing Zhang
{"title":"通过调节 JAK/STAT 信号通路敲除 miR-155 减轻慢性自发性荨麻疹大鼠的皮肤损伤","authors":"Yue-Peng An, Rui Yuan, Shan-Shan Wang, Su-Qing Yang, Qing Zhang","doi":"10.1186/s13223-024-00902-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to investigate the role and mechanisms of miR-155 in chronic spontaneous urticaria (CSU).</p><p><strong>Methods: </strong>The expression level of miR-155 in the skin tissues of patients with CSU and experimental rats were detected by RT-qPCR, followed by the measurement of the histamine release rate in the serum through the histamine release test. Besides, hematoxylin & eosin staining was used to observe the pathological changes of the skin tissues; Corresponding detection kits and flow cytometry to measure the changes of immunoglobulins, inflammatory cytokines and T cell subsets in the serum of rats in each group; and western blot to check the expression level of proteins related to JAK/STAT signaling pathway in the skin tissues.</p><p><strong>Results: </strong>Knockdown of miR-155 reduced the number and duration of pruritus, alleviated the skin damage, and decreased the number of eosinophils in CSU rats. Moreover, knockdown of miR-155 elevated the serum levels of IgG and IgM, decreased the levels of IgA and inflammatory cytokines, and reduced the proportion of CD4 + and CD4 + CD25 + T cells, as well as the CD4+/CD8 + ratio in CSU rats. However, Tyr705 intervention could reverse the effects of knockdown of miR-155 on CSU model rats. Furthermore, we found that knockdown of miR-155 significantly reduced the protein expression of IRF-9, as well as the P-JAK2/JAK2 and P-STAT3/STAT3 ratios in the skin tissues of CSU rats.</p><p><strong>Conclusion: </strong>Knockdown of miR-155 can alleviate skin damage and inflammatory responses and relieve autoimmunity in CSU rats by inhibiting the JAK/STAT3 signaling pathway.</p>","PeriodicalId":51302,"journal":{"name":"Allergy Asthma and Clinical Immunology","volume":"20 1","pages":"38"},"PeriodicalIF":2.6000,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218296/pdf/","citationCount":"0","resultStr":"{\"title\":\"Knockdown of miR-155 alleviates skin damage in rats with chronic spontaneous urticaria by modulating the JAK/STAT signaling pathway.\",\"authors\":\"Yue-Peng An, Rui Yuan, Shan-Shan Wang, Su-Qing Yang, Qing Zhang\",\"doi\":\"10.1186/s13223-024-00902-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>The aim of this study was to investigate the role and mechanisms of miR-155 in chronic spontaneous urticaria (CSU).</p><p><strong>Methods: </strong>The expression level of miR-155 in the skin tissues of patients with CSU and experimental rats were detected by RT-qPCR, followed by the measurement of the histamine release rate in the serum through the histamine release test. Besides, hematoxylin & eosin staining was used to observe the pathological changes of the skin tissues; Corresponding detection kits and flow cytometry to measure the changes of immunoglobulins, inflammatory cytokines and T cell subsets in the serum of rats in each group; and western blot to check the expression level of proteins related to JAK/STAT signaling pathway in the skin tissues.</p><p><strong>Results: </strong>Knockdown of miR-155 reduced the number and duration of pruritus, alleviated the skin damage, and decreased the number of eosinophils in CSU rats. Moreover, knockdown of miR-155 elevated the serum levels of IgG and IgM, decreased the levels of IgA and inflammatory cytokines, and reduced the proportion of CD4 + and CD4 + CD25 + T cells, as well as the CD4+/CD8 + ratio in CSU rats. However, Tyr705 intervention could reverse the effects of knockdown of miR-155 on CSU model rats. Furthermore, we found that knockdown of miR-155 significantly reduced the protein expression of IRF-9, as well as the P-JAK2/JAK2 and P-STAT3/STAT3 ratios in the skin tissues of CSU rats.</p><p><strong>Conclusion: </strong>Knockdown of miR-155 can alleviate skin damage and inflammatory responses and relieve autoimmunity in CSU rats by inhibiting the JAK/STAT3 signaling pathway.</p>\",\"PeriodicalId\":51302,\"journal\":{\"name\":\"Allergy Asthma and Clinical Immunology\",\"volume\":\"20 1\",\"pages\":\"38\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2024-06-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11218296/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Allergy Asthma and Clinical Immunology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13223-024-00902-x\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ALLERGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Allergy Asthma and Clinical Immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13223-024-00902-x","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ALLERGY","Score":null,"Total":0}
Knockdown of miR-155 alleviates skin damage in rats with chronic spontaneous urticaria by modulating the JAK/STAT signaling pathway.
Objective: The aim of this study was to investigate the role and mechanisms of miR-155 in chronic spontaneous urticaria (CSU).
Methods: The expression level of miR-155 in the skin tissues of patients with CSU and experimental rats were detected by RT-qPCR, followed by the measurement of the histamine release rate in the serum through the histamine release test. Besides, hematoxylin & eosin staining was used to observe the pathological changes of the skin tissues; Corresponding detection kits and flow cytometry to measure the changes of immunoglobulins, inflammatory cytokines and T cell subsets in the serum of rats in each group; and western blot to check the expression level of proteins related to JAK/STAT signaling pathway in the skin tissues.
Results: Knockdown of miR-155 reduced the number and duration of pruritus, alleviated the skin damage, and decreased the number of eosinophils in CSU rats. Moreover, knockdown of miR-155 elevated the serum levels of IgG and IgM, decreased the levels of IgA and inflammatory cytokines, and reduced the proportion of CD4 + and CD4 + CD25 + T cells, as well as the CD4+/CD8 + ratio in CSU rats. However, Tyr705 intervention could reverse the effects of knockdown of miR-155 on CSU model rats. Furthermore, we found that knockdown of miR-155 significantly reduced the protein expression of IRF-9, as well as the P-JAK2/JAK2 and P-STAT3/STAT3 ratios in the skin tissues of CSU rats.
Conclusion: Knockdown of miR-155 can alleviate skin damage and inflammatory responses and relieve autoimmunity in CSU rats by inhibiting the JAK/STAT3 signaling pathway.
期刊介绍：
Allergy, Asthma & Clinical Immunology (AACI), the official journal of the Canadian Society of Allergy and Clinical Immunology (CSACI), is an open access journal that encompasses all aspects of diagnosis, epidemiology, prevention and treatment of allergic and immunologic disease.
By offering a high-visibility forum for new insights and discussions, AACI provides a platform for the dissemination of allergy and clinical immunology research and reviews amongst allergists, pulmonologists, immunologists and other physicians, healthcare workers, medical students and the public worldwide.
AACI reports on basic research and clinically applied studies in the following areas and other related topics: asthma and occupational lung disease, rhinoconjunctivitis and rhinosinusitis, drug hypersensitivity, allergic skin diseases, urticaria and angioedema, venom hypersensitivity, anaphylaxis and food allergy, immunotherapy, immune modulators and biologics, immune deficiency and autoimmunity, T cell and B cell functions, regulatory T cells, natural killer cells, mast cell and eosinophil functions, complement abnormalities.
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