Journal of Neuroimmunology, Vol. 133 (1-2) (2002) pp. 30-38
Marc A.T. Teunis a, Cobi J. Heijnen a , Frans Sluyter b 1 , Joost M. Bakker a, Anne-Marie M.W. Van Dam c, Maleen Hof b, Alexander R. Cools b and Annemieke Kavelaars a
a Laboratory for Psychoneuroimmunology, Department of Immunology, Wilhelmina Children's Hospital of the University Medical Center Utrecht, Room KC03.068.0 Lundlaan 6, 3584 EA Utrecht, The Netherlands
b Department of Psychoneuropharmacology, Nijmegen Institute of Neurosciences, University of Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands
c Department of Medical Pharmacology, Research Institute Neurosciences, VU University Medical Center, Amsterdam, The Netherlands
Maternal deprivation of neonatal animals has been shown to induce long-lasting changes in the reactivity of the neuroendocrine system.
The aim of the present study was to investigate whether maternal deprivation also affects susceptibility to immune-mediated diseases such as experimental autoimmune encephalomyelitis (EAE) in adult life.
To this end, 9-day-old rat pups were subjected to a short-lasting maternal deprivation for a period of 24 h.
At the age of 8 weeks, we induced EAE in these rats by immunization with myelin basic protein (MBP) in complete Freund's adjuvant.
Our data demonstrate that short-lasting maternal deprivation induces a marked increase in the severity of EAE in the animals in later life.
The histopathological evaluation of spinal cord and cerebellum corresponded with the observed differences in clinical symptoms of EAE.
Moreover, neonatal maternal deprivation affects macrophage functioning at adult age.
In contrast, no differences were observed in in vitro mitogen- and MBP-induced cytokine production by splenocytes.
LPS-induced corticosterone release did not differ either between maternally deprived and control animals.
We conclude that short-lasting neonatal maternal deprivation of rat pups has long-lasting consequences for macrophage activity and for susceptibility to the inflammatory autoimmune disease EAE.
© 2002 Elsevier Science B.V.