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Mediators of Inflammation
Volume 2016 (2016), Article ID 6985903, 8 pages
Research Article

Differential Expression of Inflammation-Related Genes in Children with Down Syndrome

1Unit of Research in Genetics and Molecular Biology (UPGEM), Department of Molecular Biology, Medical School of São José do Rio Preto (FAMERP), 15090-000 São José do Rio Preto, SP, Brazil
2Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil
3Center for Medical Genomics at HCFMRP/USP, Ribeirão Preto, SP, Brazil
4Regional Blood of Ribeirão Preto at HCFMRP/USP, Ribeirão Preto, SP, Brazil
5Institute of Bioinformatics and Biotechnology (2bio), Ribeirão Preto, SP, Brazil
6Metrópole Digital Institute (IMD), UFRN, Natal, RN, Brazil

Received 9 March 2016; Accepted 5 April 2016

Academic Editor: Ulrich Eisel

Copyright © 2016 Cláudia Regina Santos Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. The aim of the study was to investigate the expression patterns of a specific set of genes involved in the inflammation process in children with Down Syndrome (DS) and children without the syndrome (control group) to identify differences that may be related to the immune abnormalities observed in DS individuals. Method. RNA samples were obtained from peripheral blood, and gene expression was quantified using the TaqMan® Array Plate Human Inflammation Kit, which facilitated the investigation into 92 inflammation-related genes and four reference genes using real-time polymerase chain reaction (qPCR). Results. Twenty genes showed differential expression in children with DS; 12 were overexpressed (PLA2G2D, CACNA1D, ALOX12, VCAM1, ICAM1, PLCD1, ADRB1, HTR3A, PDE4C, CASP1, PLA2G5, and PLCB4), and eight were underexpressed (LTA4H, BDKRB1, ADRB2, CD40LG, ITGAM, TNFRSF1B, ITGB1, and TBXAS1). After statistically correcting for the false discovery rate, only the genes BDKRB1 and LTA4H showed differential expression, and both were underexpressed within the DS group. Conclusion. DS children showed differential expression of inflammation-related genes that were not located on chromosome 21 compared with children without DS. The BDKRB1 and LTA4H genes may differentiate the case and control groups based on the inflammatory response, which plays an important role in DS pathogenesis.