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Departments of
*
Pediatric Immunology and
Neonatology, Wilhelmina Children’s Hospital of the University Medical Center, and
Rudolf Magnus Institute, Utrecht, The Netherlands
Major concern has emerged about the possible long term adverse
effects of glucocorticoid treatment, which is frequently used for the
prevention of chronic lung disease in preterm infants. Here we show
that neonatal glucocorticoid treatment of rats increases the severity
(p 
0.01) and incidence (p
0.01) of the inflammatory autoimmune disease experimental autoimmune
encephalomyelitis in adult life. In search of possible mechanisms
responsible for the increased susceptibility to experimental autoimmune
encephalomyelitis, we investigated the reactivity of the
hypothalamo-pituitary-adrenal axis and of immune cells in adult rats
after neonatal glucocorticoid treatment. We observed that neonatal
glucocorticoid treatment reduces the corticosterone response after an
LPS challenge in adult rats (p 0.001).
Interestingly, LPS-stimulated macrophages of glucocorticoid-treated
rats produce less TNF-
and IL-1
in adult life than control rats
(p < 0.05). In addition, splenocytes obtained from
adult rats express increased mRNA levels of the proinflammatory
cytokines IFN-
(p < 0.01) and TNF-
(p < 0.05) after neonatal glucocorticoid
treatment. Apparently, neonatal glucocorticoid treatment has permanent
programming effects on endocrine as well as immune functioning in adult
life. In view of the frequent clinical application of glucocorticoids
to preterm infants, our data demonstrate that neonatal glucocorticoid
treatment may be a risk factor for the development of (auto)immune
disease in man.
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