The transcriptional profile of coronary arteritis in Kawasaki disease Journal Article

Authors: Rowley, A. H.; Wylie, K. M.; Kim, K. Y.; Pink, A. J.; Yang, A.; Reindel, R; Baker, S. C.; Shulman, S. T.; Orenstein, J. M.; Lingen, M. W.; Weinstock, G. M.; Wylie, T. N.
Article Title: The transcriptional profile of coronary arteritis in Kawasaki disease
Abstract: BACKGROUND: Kawasaki Disease (KD) can cause potentially life-threatening coronary arteritis in young children, and has a likely infectious etiology. Transcriptome profiling is a powerful approach to investigate gene expression in diseased tissues. RNA sequencing of KD coronary arteries could elucidate the etiology and the host response, with the potential to improve KD diagnosis and/or treatment. METHODS: Deep RNA sequencing was performed on KD (n = 8) and childhood control (n = 7) coronary artery tissues, revealing 1074 differentially expressed mRNAs. Non-human RNA sequences were subjected to a microbial discovery bioinformatics platform, and microbial sequences were analyzed by Metastats for association with KD. RESULTS: T lymphocyte activation, antigen presentation, immunoglobulin production, and type I interferon response were significantly upregulated in KD arteritis, while the tumor necrosis factor alpha pathway was not differentially expressed. Transcripts from known infectious agents were not specifically associated with KD coronary arteritis. CONCLUSIONS: The immune transcriptional profile in KD coronary artery tissues has features of an antiviral immune response such as activated cytotoxic T lymphocyte and type I interferon-induced gene upregulation. These results provide new insights into the pathogenesis of KD arteritis that can guide selection of new immunomodulatory therapies for high-risk KD patients, and provide direction for future etiologic studies.
Journal Title: BMC genomics
Volume: 16
Issue: 1
ISSN: 1471-2164; 1471-2164
Publisher: Unknown  
Journal Place: England
Date Published: 2015
Start Page: 1076
End Page: 015-2323-5
Language: eng
Notes: LR: 20160120; GR: UL1 TR001422/TR/NCATS NIH HHS/United States; JID: 100965258; OID: NLM: PMC4683744; 2015/06/25 [received]; 2015/12/15 [accepted]; 2015/12/18 [aheadofprint]; epublish