Insulin-like growth factor-I regulates the neonatal immune response in infection and maturation by suppression of IFN-γ

Alexander Puzik*, Jan Rupp, Birte Tröger, Wolfgang Göpel, Egbert Herting, Christoph Härtel

*Korrespondierende/r Autor/-in für diese Arbeit
11 Zitate (Scopus)

Abstract

Disturbances in Insulin-like growth factor-I (IGF-I) and dysregulation in neonatal immune responses have been associated with typical neonatal diseases. Immunosuppression by IGF-I might be a key regulator of neonatal immune responses in infection and maturation. However, information on IGF-I serum levels, IGF-I-receptor (IGF-IR) and effects on functional properties of neonatal immune cells is scarce. Neonatal cord blood samples were stimulated with anti-CD3/anti-CD28, PMA/ionomycin or LPS in a whole-blood assay, while IGF-I serum levels and IGF-I receptor expression were assessed. Furthermore the effect of IGF-I on cytokine expression, apoptosis and the DNA binding activity of AP-1 and NFκB was evaluated. IGF-I serum levels were within normal range. The IGF-I-receptor was present on the surface of cord blood CD3. +. CD4. +. lymphocytes and cord blood CD14. +. monocytes. Upon stimulation the IGF-I-R expression on lymphocytes was significantly upregulated. The addition of IGF-I (100. ng/ml) to whole blood cultures inhibited the secretion of IFN-γ from PMA/ionomycin-stimulated cord blood mononuclear cells (CBMC). While IGF-I did not influence apoptosis in our experimental setting, it led to a distinct decrease in anti-CD3/CD28-stimulated DNA binding activity of AP-1 and NFκB. Thus IGF-I may be a key regulator of neonatal immune responses in maturation processes and inflammation by suppressing proinflammatory Th1 responses. Future in vivo studies need to elucidate whether disturbances of the IGF-I serum level and IGF-IR expression are associated with susceptibility for infections and subsequent diseases in neonates.

OriginalspracheEnglisch
ZeitschriftCytokine
Jahrgang60
Ausgabenummer2
Seiten (von - bis)369-376
Seitenumfang8
ISSN1043-4666
DOIs
PublikationsstatusVeröffentlicht - 01.11.2012

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