Seminars in Fetal & Neonatal Medicine
Volume 12, Issue 4 , Pages 280-286, August 2007

Inflammation-induced preconditioning in the immature brain

  • Carina Mallard

      Affiliations

    • Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy, Göteborg University, Box 432, 40530 Göteborg, Sweden
    • Corresponding Author InformationCorresponding author. Tel.: +46 31 773 3498; fax: +46 31 773 3512.
    • ,
  • Henrik Hagberg

      Affiliations

    • Department of Obstetrics and Gynecology, Sahlgrenska Academy, Göteborg University, Box 432, 40530 Göteborg, Sweden

published online 28 February 2007.

Summary 

Infections are important risk factors of perinatal brain injury. However, under certain circumstances, inflammation mediates preconditioning and provides protection to the immature brain. Recent experimental studies have examined the interaction of lipopolysaccharide (LPS) with other events. Evidence demonstrates that LPS administered 24h before hypoxia–ischemia in 7-day-old rats provides neuroprotection, which is associated with up-regulation of endogenous corticosterone but is also linked to significant cerebral gene regulation. Gene ontology analysis reveals that the most over-represented genes belong to immune and inflammatory processes. However, a number of cell death/survival genes, including complement component 1, complement component 3, aquaporin 4, epidermal growth factor receptor pathway substrate 15 and PYD and CARD domain containing are also significantly up-regulated 24h following LPS exposure. These results suggest that in addition to immune-related activation, transcription of cell death pathways may be important in LPS-induced preconditioning in the immature brain.

Keywords: Hypoxia–ischemia, Immature brain, LPS, Preconditioning

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PII: S1744-165X(07)00015-7

doi:10.1016/j.siny.2007.01.014

Seminars in Fetal & Neonatal Medicine
Volume 12, Issue 4 , Pages 280-286, August 2007

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