Youngsoo Lee, Jin Young Noh, Jiwon Yoon, Boyoun Choi, JungMo Kim, Hyun Goo Woo, Young-Min Ye
{"title":"慢性自发性荨麻疹患者MicroRNA表达差异与治疗反应的关系","authors":"Youngsoo Lee, Jin Young Noh, Jiwon Yoon, Boyoun Choi, JungMo Kim, Hyun Goo Woo, Young-Min Ye","doi":"10.4168/aair.2026.18.2.271","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disorder characterized by a complex pathogenesis involving immune dysregulation and inflammation. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators in various diseases. This study aimed to investigate differentially expressed serum miRNAs in CSU and its association with treatment response.</p><p><strong>Methods: </strong>Thirty CSU patients (37.9 ± 9.8 years, 15 females) and 10 normal controls were enrolled. Patients were stratified by clinical response to H₁-antihistamines (H1AHs) and omalizumab. Serum miRNAs were profiled using the Affymetrix GeneChip<sup>®</sup> miRNA 4.0 Array. Differentially expressed miRNAs were identified, and bioinformatic analyses were performed to predict target genes and assess pathway enrichment.</p><p><strong>Results: </strong>Eighteen miRNAs were differentially expressed between CSU patients and normal controls, with 10 upregulated and 8 downregulated in CSU. Compared to H1AH responders, 23 miRNAs were downregulated in H1AH nonresponders. In omalizumab-treated patients, 4 miRNAs, hsa-miR-503-5p, hsa-miR-1282, hsa-miR-93-5p, and hsa-miR-638, were reduced in complete responders. Bioinformatic analysis identified 3 hub genes (MYC proto-oncogene [<i>MYC</i>], cyclin D1 [<i>CCND1</i>], ribonucleotide reductase regulatory subunit M2) in H1AH nonresponse, and 14 key target genes, including heat shock protein family A (Hsp70) member 8 (<i>HSPA8</i>), <i>CCND1</i>, and E2F transcription factor 3, in omalizumab complete responders. Notably, hsa-miR-93-5p and its predicted target <i>CCND1</i> were associated with both H1AH nonresponsiveness and omalizumab complete response.</p><p><strong>Conclusions: </strong>Distinct serum miRNA signatures are associated with treatment responses in CSU. In particular, miR-93-5p with network targets, including <i>MYC</i>, <i>CCND1</i>, and <i>HSPA8</i>, indicates shared regulatory pathways underlying H1AH refractoriness and omalizumab responsiveness. These findings offer mechanistic insights into CSU pathogenesis and support a personalized approach to treatment.</p>","PeriodicalId":7547,"journal":{"name":"Allergy, Asthma & Immunology Research","volume":"18 2","pages":"271-285"},"PeriodicalIF":4.3000,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13047436/pdf/","citationCount":"0","resultStr":"{\"title\":\"Differential MicroRNA Expression in Chronic Spontaneous Urticaria in Relation to Treatment Response.\",\"authors\":\"Youngsoo Lee, Jin Young Noh, Jiwon Yoon, Boyoun Choi, JungMo Kim, Hyun Goo Woo, Young-Min Ye\",\"doi\":\"10.4168/aair.2026.18.2.271\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disorder characterized by a complex pathogenesis involving immune dysregulation and inflammation. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators in various diseases. This study aimed to investigate differentially expressed serum miRNAs in CSU and its association with treatment response.</p><p><strong>Methods: </strong>Thirty CSU patients (37.9 ± 9.8 years, 15 females) and 10 normal controls were enrolled. Patients were stratified by clinical response to H₁-antihistamines (H1AHs) and omalizumab. Serum miRNAs were profiled using the Affymetrix GeneChip<sup>®</sup> miRNA 4.0 Array. Differentially expressed miRNAs were identified, and bioinformatic analyses were performed to predict target genes and assess pathway enrichment.</p><p><strong>Results: </strong>Eighteen miRNAs were differentially expressed between CSU patients and normal controls, with 10 upregulated and 8 downregulated in CSU. Compared to H1AH responders, 23 miRNAs were downregulated in H1AH nonresponders. In omalizumab-treated patients, 4 miRNAs, hsa-miR-503-5p, hsa-miR-1282, hsa-miR-93-5p, and hsa-miR-638, were reduced in complete responders. Bioinformatic analysis identified 3 hub genes (MYC proto-oncogene [<i>MYC</i>], cyclin D1 [<i>CCND1</i>], ribonucleotide reductase regulatory subunit M2) in H1AH nonresponse, and 14 key target genes, including heat shock protein family A (Hsp70) member 8 (<i>HSPA8</i>), <i>CCND1</i>, and E2F transcription factor 3, in omalizumab complete responders. Notably, hsa-miR-93-5p and its predicted target <i>CCND1</i> were associated with both H1AH nonresponsiveness and omalizumab complete response.</p><p><strong>Conclusions: </strong>Distinct serum miRNA signatures are associated with treatment responses in CSU. In particular, miR-93-5p with network targets, including <i>MYC</i>, <i>CCND1</i>, and <i>HSPA8</i>, indicates shared regulatory pathways underlying H1AH refractoriness and omalizumab responsiveness. These findings offer mechanistic insights into CSU pathogenesis and support a personalized approach to treatment.</p>\",\"PeriodicalId\":7547,\"journal\":{\"name\":\"Allergy, Asthma & Immunology Research\",\"volume\":\"18 2\",\"pages\":\"271-285\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2026-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13047436/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Allergy, Asthma & Immunology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.4168/aair.2026.18.2.271\",\"RegionNum\":2,\"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 & Immunology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4168/aair.2026.18.2.271","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ALLERGY","Score":null,"Total":0}
Differential MicroRNA Expression in Chronic Spontaneous Urticaria in Relation to Treatment Response.
Purpose: Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disorder characterized by a complex pathogenesis involving immune dysregulation and inflammation. MicroRNAs (miRNAs) have emerged as critical post-transcriptional regulators in various diseases. This study aimed to investigate differentially expressed serum miRNAs in CSU and its association with treatment response.
Methods: Thirty CSU patients (37.9 ± 9.8 years, 15 females) and 10 normal controls were enrolled. Patients were stratified by clinical response to H₁-antihistamines (H1AHs) and omalizumab. Serum miRNAs were profiled using the Affymetrix GeneChip® miRNA 4.0 Array. Differentially expressed miRNAs were identified, and bioinformatic analyses were performed to predict target genes and assess pathway enrichment.
Results: Eighteen miRNAs were differentially expressed between CSU patients and normal controls, with 10 upregulated and 8 downregulated in CSU. Compared to H1AH responders, 23 miRNAs were downregulated in H1AH nonresponders. In omalizumab-treated patients, 4 miRNAs, hsa-miR-503-5p, hsa-miR-1282, hsa-miR-93-5p, and hsa-miR-638, were reduced in complete responders. Bioinformatic analysis identified 3 hub genes (MYC proto-oncogene [MYC], cyclin D1 [CCND1], ribonucleotide reductase regulatory subunit M2) in H1AH nonresponse, and 14 key target genes, including heat shock protein family A (Hsp70) member 8 (HSPA8), CCND1, and E2F transcription factor 3, in omalizumab complete responders. Notably, hsa-miR-93-5p and its predicted target CCND1 were associated with both H1AH nonresponsiveness and omalizumab complete response.
Conclusions: Distinct serum miRNA signatures are associated with treatment responses in CSU. In particular, miR-93-5p with network targets, including MYC, CCND1, and HSPA8, indicates shared regulatory pathways underlying H1AH refractoriness and omalizumab responsiveness. These findings offer mechanistic insights into CSU pathogenesis and support a personalized approach to treatment.
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The journal features cutting-edge original research, brief communications, and state-of-the-art reviews in the specialties of allergy, asthma, and immunology, including clinical and experimental studies and instructive case reports. Contemporary reviews summarize information on topics for researchers and physicians in the fields of allergy and immunology. As of January 2017, AAIR do not accept case reports. However, if it is a clinically important case, authors can submit it in the form of letter to the Editor. Editorials and letters to the Editor explore controversial issues and encourage further discussion among physicians dealing with allergy, immunology, pediatric respirology, and related medical fields. AAIR also features topics in practice and management and recent advances in equipment and techniques for clinicians concerned with clinical manifestations of allergies and pediatric respiratory diseases.
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