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Neurosci Lett. 2010 Aug 16;480(2):122-6. doi: 10.1016/j.neulet.2010.06.021. Epub 2010 Jun 11.

Interleukin-2 as a neuromodulator possibly implicated in the physiopathology of sudden infant death syndrome.

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  • 1Neuropathology Unit, Department of Anatomic Pathology, Centre Hospitalier Universitaire Brugmann, Université Libre de Bruxelles (U.L.B.), Place van Gehuchten 4, 1020 Brussels, Belgium. Hazim.Kadhim@chu-brugmann.be

Abstract

Dysfunction in vital brainstem centers, including those controlling cardiorespiratory- and sleep/arousal pathophysiology, is reported in sudden infant death syndrome (SIDS). Biological mechanisms underlying SIDS, however, remain unclear. Cytokines are inter-cellular signaling chemicals. They can interact with neurotransmitters and might thus modify neural and neuroimmune functions. Cytokines could therefore act as neuromodulators. Interleukin (IL)-2 is a major immune-related cytokine. It has not been previously depicted in vital brainstem centers. We detected intense neuronal IL-2 immune-reactivity in the SIDS brainstem, namely in vital neural centers. This IL-2 overexpression might interfere with neurotransmitters in those critical brainstem centers, causing disturbed homeostatic control of cardiorespiratory and arousal responses, possibly leading to SIDS.

PMID:
20542085
DOI:
10.1016/j.neulet.2010.06.021
[PubMed - indexed for MEDLINE]
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