Misregulation of suppressors of cytokine signaling in eosinophilic esophagitis

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• 作者：Ma Paz Zafra (1) (6)
  Natally Cancelliere (2)
  Pablo Rodríguez del Río (3)
  Mónica Ruiz-García (4)
  Laura Estévez (1)
  Victoria Andregnette (4)
  Silvia Sánchez-García (3)
  Ana Fiandor (2)
  Elena Collantes (5)
  Joaquín Sastre (4) (6)
  Santiago Quirce (2) (6)
  María Dolores Ibá?ez (3)
  Victoria del Pozo (1) (6)
  
• 关键词：SOCS1 ; SOCS3 ; Eosinophilic esophagitis
• 刊名：Journal of Gastroenterology
• 出版年：2013
• 出版时间：August 2013
• 年：2013
• 卷：48
• 期：8
• 页码：910-920
• 全文大小：462KB
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• 作者单位：Ma Paz Zafra (1) (6)
  Natally Cancelliere (2)
  Pablo Rodríguez del Río (3)
  Mónica Ruiz-García (4)
  Laura Estévez (1)
  Victoria Andregnette (4)
  Silvia Sánchez-García (3)
  Ana Fiandor (2)
  Elena Collantes (5)
  Joaquín Sastre (4) (6)
  Santiago Quirce (2) (6)
  María Dolores Ibá?ez (3)
  Victoria del Pozo (1) (6)
  
  1. Department of Immunology, Fundación Jiménez Díaz-Capio, Av. Reyes Católicos 2, 28040, Madrid, Spain
  6. CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain
  2. Department of Allergy, Hospital La Paz Health Research Institute (IdiPAZ), Madrid, Spain
  3. Department of Allergy, Hospital Infantil Universitario del Ni?o Jesus, Madrid, Spain
  4. Department of Allergy, Fundación Jiménez Díaz-Capio, Madrid, Spain
  5. Department of Pathology, Hospital La Paz Health Research Institute (IdiPAZ), Madrid, Spain
  

文摘

Background Several findings suggest that eosinophilic esophagitis (EoE) is strongly associated with atopy and allergen-driven, Th2-type immune responses, indicating the association of EoE with immune dysregulation. The objective of this study is to ascertain the molecular mechanism involved in EoE disease development a Th2 condition. Methods 25 patients with diagnosis of EoE and 17 non-EoE controls were recruited by the gastroenterology and allergy departments from three different hospitals. Transcription analysis of suppressors of cytokine signaling 1, 3, 5 (SOCS), interleukin-5 (IL), IL-13, eotaxin (CCL26), eoataxin receptor (CCR3), and mitogen-activated protein kinase 1 (MAPK1) was performed in esophageal biopsies by real time PCR. Western blot of ERK esophageal protein and additional measures of IL-5 and VEGF levels in serum were performed. Results The esophagus of EoE patients expresses and synthesizes high levels of SOCS1 and SOCS3 proteins (P?<?0.05), and these expression correlated with levels of IL-5, IL-13, CCL26, CCR3, and MAPK1 genes. In addition, we demonstrate the implication of the ERK pathway (P?<?0.001). Conclusions SOCS proteins probably contribute to EoE pathogenesis by directly or indirectly inducing the Th2 profile, as well as by promoting the production of Th2 cytokines. All these findings further enhance our understanding of the mechanism of EoE, and accumulating evidence suggests that EoE pathogenesis is likely to be due to misregulation of immunological pathways.