Display Settings:

Format

Send to:

Choose Destination
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.

Author information

  • 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.

Copyright 2010 Elsevier Ireland Ltd. All rights reserved.

PMID:
20542085
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk