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

被引:9
作者
Kadhim, Hazim [1 ,2 ]
Deltenre, Paul [3 ]
De Prez, Carine [4 ]
Sebire, Guillaume [5 ]
机构
[1] Univ Libre Bruxelles, Neuropathol Unit, Dept Anat Pathol, Ctr Hosp Univ Brugmann, B-1020 Brussels, Belgium
[2] Univ Libre Bruxelles, Dept Biol Clin, Ctr Hosp Univ Brugmann, B-1020 Brussels, Belgium
[3] Univ Libre Bruxelles, Dept Neurol, Ctr Hosp Univ Brugmann, B-1020 Brussels, Belgium
[4] Univ Libre Bruxelles, Dept Pathol, Ctr Hosp Univ Brugmann, B-1020 Brussels, Belgium
[5] Univ Sherbrooke, Dept Pediat, Div Pediat Neurol, CHU Fleurimont, Quebec City, PQ, Canada
关键词
Sudden infant death syndrome (SIDS); Cytokines; Brain; Interleukin (IL)-2; PERIVENTRICULAR LEUKOMALACIA; INFLAMMATORY CYTOKINES; QT INTERVAL; BRAIN; VICTIMS; PROLONGATION; PATHOGENESIS; EXPRESSION; NEURONS; CELLS;
D O I
10.1016/j.neulet.2010.06.021
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:122 / 126
页数:5
相关论文
共 25 条
[1]  
CARPENTER MB, 1983, HUMAN NEUROANATOMY, P811
[2]   Auto/paracrine control of inflammatory cytokines by acetylcholine in macrophage-like U937 cells through nicotinic receptors [J].
Chernyavsky, Alexander I. ;
Arredondo, Juan ;
Skok, Maryna ;
Grando, Sergei A. .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2010, 10 (03) :308-315
[3]  
FILIANO JJ, 1994, BIOL NEONATE, V65, P194
[4]   Decreased autonomic responses to obstructive sleep events in future victims of sudden infant death syndrome [J].
Franco, P ;
Szliwowski, H ;
Dramaix, M ;
Kahn, A .
PEDIATRIC RESEARCH, 1999, 46 (01) :33-39
[5]   QT Interval Prolongation in Future SIDS Victims: A Polysomnographic Study [J].
Franco, Patricia ;
Groswasser, Jose ;
Scaillet, Sonia ;
Lanquart, Jean-Pol ;
Benatar, Abraham ;
Sastre, Jean-Pierre ;
Chevalier, Philippe ;
Kugener, Beatrice ;
Kahn, Andre ;
Lin, Jian-Sheng .
SLEEP, 2008, 31 (12) :1691-1699
[6]   Adverse effects of nicotine and interleukin-1β on autoresuscitation after apnea in piglets:: Implications for sudden infant death syndrome [J].
Froen, TF ;
Aker, H ;
Stray-Pedersen, B ;
Saugstad, OD .
PEDIATRICS, 2000, 105 (04)
[7]   The triple risk hypotheses in sudden infant death syndrome [J].
Guntheroth, WG ;
Spiers, PS .
PEDIATRICS, 2002, 110 (05) :e64
[8]   In situ detection of intracerebral cytokine expression after human brain contusion [J].
Holmin, S ;
Höjeberg, B .
NEUROSCIENCE LETTERS, 2004, 369 (02) :108-114
[9]   Incongruent cerebral growth in sudden infant death syndrome [J].
Kadhim, H ;
Sébire, G ;
Khalifa, M ;
Evrard, P ;
Groswasser, J ;
Franco, P ;
Kahn, A .
JOURNAL OF CHILD NEUROLOGY, 2005, 20 (03) :244-246
[10]   Distinct cytokine profile in SIDS brain -: A common denominator in a multifactorial syndrome? [J].
Kadhim, H ;
Kahn, A ;
Sébire, G .
NEUROLOGY, 2003, 61 (09) :1256-1259