Interleukin-2 as a neuromodulator possibly implicated in the physiopathology of sudden infant death syndrome.
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.
Kadhim
Hazim
H
Neuropathology 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
Deltenre
Paul
P
De Prez
Carine
C
Sébire
Guillaume
G
D001933:Brain Stem / Q000378:metabolism* / Q000473:pathology; D005260:Female; D006801:Humans; D007223:Infant; D007376:Interleukin-2 / Q000378:metabolism*; D008297:Male; D015213:Neuroimmunomodulation; D013398:Sudden Infant Death / Q000276:immunology* / Q000473:pathology
D007376:Interleukin-2