Neurology 2002;58:446-451
© 2002 American Academy of Neurology
Release of soluble ICAM-5, a neuronal adhesion molecule, in acute encephalitis
P. J. Lindsberg, MD*;,
J. Launes, MD*;,
L. Tian, M.Med*;,
H. Välimaa, MD,
V. Subramanian, MSc,
J. Sirén, MD,
L. Hokkanen, PhD,
T. Hyypiä, MD,
O. Carpén, MD and
C. G. Gahmberg, MD
*All of these authors contributed equally to this work.
From the Department of Neurology (Drs. Lindsberg, Launes, Sirén, and Hokkanen), Helsinki University Central Hospital, and the Neuroscience Program (Drs. Lindsberg and Carpén), Biomedicum Helsinki, University of Helsinki; Department of Biosciences (Dr. Gahmberg, L. Tian, and V. Subramanian), Division of Biochemistry, University of Helsinki; Departments of Cardiology and Virology (Dr. Välimaa), University of Turku, Finland; and Departments of Virology (Drs. Välimaa and Hyypiä) and Pathology (Dr. Carpén), Haartman Institute, University of Helsinki, Finland.
Address correspondence and reprint requests to Dr. Perttu J. Lindsberg, Neuroscience Program, Biomedicum Helsinki, P.O. Box 700, FIN-00029 HUS, Finland; e-mail: perttu.lindsberg{at}hus.fi
Background: Intercellular adhesion molecule (ICAM)-5 (telencephalin) is an adhesion molecule in telencephalic neurons of the mammalian brain that binds to the leukocyte integrin CD11a/CD18. The authors observed that human cerebral neurons also expressed ICAM-5 and that ICAM-5–mediated neuron–leukocyte binding in cultured hippocampal neurons. This led the authors to examine ICAM-5 expression during clinical CNS inflammation.
Methods: The authors found, by immunoblotting, a 115-kDa soluble form of ICAM-5 (sICAM-5) cleaved from the membrane-bound (130 kDa) ICAM-5, and established an ELISA assay to measure it. CSF samples of patients with acute encephalitis and MS were studied.
Results: sICAM-5 was increased in encephalitis (320 ± 107 ng/mL; n = 25), as compared with patients with MS (128 ± 10 ng/mL; n = 16) and control subjects without CNS disease (137 ± 6 ng/mL; n = 42) (p < 0.001). The concentration of sICAM-5 correlated with the performance in the immediate recall task (p = 0.013) and with the leukocyte count in the CSF (p = 0.02), especially in cases caused by herpes simplex virus (HSV) (r = 0.94; p = 0.002).
Conclusions: sICAM-5 is cleaved from CNS into CSF during acute encephalitis, and it may mediate leukocyte–neuron interactions. sICAM-5 release from cerebral neurons may actively regulate immune responses and leukocyte adhesion during microbial neuroinvasion in humans during encephalitis.
This article has been cited by other articles:
|
|
|
|
 
X. Wu, Q. Liu, and R. Jiang
Align human interactome with phenome to identify causative genes and networks underlying disease families
Bioinformatics,
January 1, 2009;
25(1):
98 - 104.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Tian, J. Lappalainen, M. Autero, S. Hanninen, H. Rauvala, and C. G. Gahmberg
Shedded neuronal ICAM-5 suppresses T-cell activation
Blood,
April 1, 2008;
111(7):
3615 - 3625.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Tian, M. Stefanidakis, L. Ning, P. Van Lint, H. Nyman-Huttunen, C. Libert, S. Itohara, M. Mishina, H. Rauvala, and C. G. Gahmberg
Activation of NMDA receptors promotes dendritic spine development through MMP-mediated ICAM-5 cleavage
J. Cell Biol.,
August 9, 2007;
178(4):
687 - 700.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Mitsui, M. Saito, K. Mori, and Y. Yoshihara
A Transcriptional Enhancer That Directs Telencephalon-Specific Transgene Expression in Mouse Brain
Cereb Cortex,
March 1, 2007;
17(3):
522 - 530.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Nyman-Huttunen, L. Tian, L. Ning, and C. G. Gahmberg
{alpha}-Actinin-dependent cytoskeletal anchorage is important for ICAM-5-mediated neuritic outgrowth
J. Cell Sci.,
August 1, 2006;
119(15):
3057 - 3066.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. L. Huff, L. M. Hansen, and J. V. Solnick
Gastric Transcription Profile of Helicobacter pylori Infection in the Rhesus Macaque
Infect. Immun.,
September 1, 2004;
72(9):
5216 - 5226.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
