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BMC Genomics. 2015 Dec 18;16:1076. doi: 10.1186/s12864-015-2323-5.

The transcriptional profile of coronary arteritis in Kawasaki disease.

Author information

1
Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E Superior Street, Morton 4-685B, Chicago, IL, 60611, USA. a-rowley@northwestern.edu.
2
Department of Microbiology and Immunology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. a-rowley@northwestern.edu.
3
Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, USA. a-rowley@northwestern.edu.
4
Department of Pediatrics, Washington University School of Medicine, Saint Louis, MO, USA.
5
The McDonnell Genome Institute at Washington University, Washington University School of Medicine, Saint Louis, MO, USA.
6
Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
7
Department of Pediatrics, Northwestern University Feinberg School of Medicine, 310 E Superior Street, Morton 4-685B, Chicago, IL, 60611, USA.
8
Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, USA.
9
Present address: AbbVie, Inc, North Chicago, IL, USA.
10
Department of Microbiology/Immunology, Loyola University Stritch School of Medicine, Maywood, IL, USA.
11
Department of Pathology, George Washington University School of Medicine, Washington, DC, USA.
12
Department of Pathology, University of Chicago Pritzker School of Medicine, Chicago, IL, USA.
13
Present address: The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.

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 α 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.

PMID:
26679344
PMCID:
PMC4683744
DOI:
10.1186/s12864-015-2323-5
[Indexed for MEDLINE]
Free PMC Article

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