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ORIGINAL ARTICLE: The Transcriptome of the Fetal Inflammatory Response Syndrome

Authors

  • Sally A. Madsen-Bouterse,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
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  • Roberto Romero,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Obstetrics and Gynecology, Wayne State University/Hutzel Women’s Hospital, Detroit, MI, USA
    3. Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI, USA
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  • Adi L. Tarca,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Computer Science, Wayne State University, Detroit, MI, USA
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  • Juan Pedro Kusanovic,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Obstetrics and Gynecology, Wayne State University/Hutzel Women’s Hospital, Detroit, MI, USA
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  • Jimmy Espinoza,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Obstetrics and Gynecology, Wayne State University/Hutzel Women’s Hospital, Detroit, MI, USA
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  • Chong Jai Kim,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Pathology, Wayne State University, Detroit, MI, USA
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  • Jung-Sun Kim,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
    2. Department of Pathology, Wayne State University, Detroit, MI, USA
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  • Samuel S. Edwin,

    1. Perinatology Research Branch, NICHD/NIH/DHHS, Bethesda, MD, and Detroit, MI, USA
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  • Ricardo Gomez,

    1. CEDIP (Center for Perinatal Diagnosis and Research), Department of Obstetrics and Gynecology, Sotero del Rio Hospital, Pontificia Universidad Catolica de Chile, Santiago, Chile
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  • Sorin Draghici

    1. Department of Computer Science, Wayne State University, Detroit, MI, USA
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Roberto Romero, Perinatology Research Branch, NICHD, NIH, DHHS, Wayne State University/Hutzel Women’s Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA.
E-mail: prbchiefstaff@med.wayne.edu

Abstract

Problem  The fetal inflammatory response syndrome (FIRS) is considered the counterpart of the systemic inflammatory response syndrome (SIRS), but similarities in their regulatory mechanisms are unclear. This study characterizes the fetal mRNA transcriptome of peripheral leukocytes to identify key biological processes and pathways involved in FIRS.

Method of study  Umbilical cord blood from preterm neonates with FIRS (funisitis, plasma IL-6 >11 pg/mL; n = 10) and neonates with no evidence of inflammation (n = 10) was collected at birth.

Results  Microarray analysis of leukocyte RNA revealed differential expression of 541 unique genes, changes confirmed by qRT-PCR for 41 or 44 genes tested. Similar to SIRS and sepsis, ontological and pathway analyses yielded significant enrichment of biological processes including antigen processing and presentation, immune response, and processes critical to cellular metabolism. Results are comparable with microarray studies of endotoxin challenge models and pediatric sepsis, identifying 25 genes across all studies.

Conclusion  This study is the first to profile genome-wide expression in FIRS, which demonstrates a substantial degree of similarity with SIRS despite differences in fetal and adult immune systems.

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