HUMAN β -DEFENSIN 2 ISOFORMS EXPRESSION ON PEDIATRIC IBD

Inflammatory bowel disease (IBD), which includes Ulcerative Colitis (UC) and Chron’s disease, affects a million people around the world. IBD is developed during the different stages of human life and has mostly been studied in adults. However, this disease has been observed in childhood. In the case...

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Bibliographic Details
Published in:Inflammatory bowel diseases Vol. 30; no. Supplement_1; pp. S42 - S43
Main Authors: Martinez, Evelyn Calderon, Ng, Wern Lynn, Joseph, Maria, Guzman, Adalberto, Chávez, Luis Márquez, Htoo, Moe, Zevallos-Delgado, Christian
Format: Journal Article
Language:English
Published: 25-01-2024
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Summary:Inflammatory bowel disease (IBD), which includes Ulcerative Colitis (UC) and Chron’s disease, affects a million people around the world. IBD is developed during the different stages of human life and has mostly been studied in adults. However, this disease has been observed in childhood. In the case of pediatric IBD, the causes are mostly related to genetic disorders. Human β-defensin 2 isoforms (DEFB4A and DEFB4B) are one of the families strongly related to the development of multiple diseases such as asthma and colorectal cancer. The main purpose of this study was to determine the factors that can affect the progression of pediatric IBD. Using gene expression data from 190 pediatric patients (Control= 55 samples, CD = 92 samples, and UC= 43 samples) available at the Gene Expression Omnibus (Accession code = GSE117993), the differential gene expression was determined using GEO2R tool (significant level cut-ff = 0.05 and Log 2-fold threshold= 2). The results showed that DEFB4A/B were upregulated when comparing UC and CD with Control. On the other hand, DEFB4A/B was downregulated compared to CD with UC. Human β-defensin 2 isoforms have been strongly related to the development of multiple diseases, including IBD in adult patients. In the case of pediatric patients, these isoforms could represent a potential maker to assess the progression of IBD.
ISSN:1078-0998
1536-4844
DOI:10.1093/ibd/izae020.088