Abstract
Background: Although the etiopathology of autism spectrum disorder (ASD) is not clear, there is increasing evidence that dysfunction in the immune system affects many children with ASD. Findings of immune dysfunction in ASD include increases in inflammatory cytokines, chemokines, and microglial activity in brain tissue and cerebrospinal fluid, as well as abnormal peripheral immune cell function. Methods: Adhesion molecules, such as platelet endothelial adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilitate leukocyte transendothelial migration. We assessed concentrations of soluble adhesion molecules, sPECAM-1, sICAM-1, sVCAM-1, sP-selectin, and sL-selectin in the plasma of 49 participants with ASD and 31 typically developing controls of the same age, all of whom were enrolled as part of the Autism Phenome Project. Behavioral assessment, the levels of soluble adhesion molecules, and head circumference were compared in the same subjects. Results: Levels of sPECAM-1 and sP-selectin were significantly reduced in the ASD group compared to typically developing controls (p <.02). Soluble PECAM-1 levels were negatively associated with repetitive behavior and abnormal brain growth in children with ASD (p =.03). Conclusions: Because adhesion molecules modulate the permeability and signaling at the blood-brain barrier as well as leukocyte infiltration into the central nervous system, the current data suggest a role for these molecules in the complex pathophysiology of ASD.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1020-1025 |
| Number of pages | 6 |
| Journal | Biological Psychiatry |
| Volume | 72 |
| Issue number | 12 |
| DOIs | |
| State | Published - Dec 15 2012 |
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Keywords
- Adhesion
- autism
- CD31
- CD62-P
- P-Selectin
- PECAM-1
ASJC Scopus subject areas
- Biological Psychiatry
Cite this
Levels of soluble platelet endothelial cell adhesion molecule-1 and P-selectin are decreased in children with autism spectrum disorder. / Onore, Charity E.; Nordahl, Christine W; Young, Gregory S.; Van de Water, Judith A; Rogers, Sally J; Ashwood, Paul.
In: Biological Psychiatry, Vol. 72, No. 12, 15.12.2012, p. 1020-1025.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Levels of soluble platelet endothelial cell adhesion molecule-1 and P-selectin are decreased in children with autism spectrum disorder
AU - Onore, Charity E.
AU - Nordahl, Christine W
AU - Young, Gregory S.
AU - Van de Water, Judith A
AU - Rogers, Sally J
AU - Ashwood, Paul
PY - 2012/12/15
Y1 - 2012/12/15
N2 - Background: Although the etiopathology of autism spectrum disorder (ASD) is not clear, there is increasing evidence that dysfunction in the immune system affects many children with ASD. Findings of immune dysfunction in ASD include increases in inflammatory cytokines, chemokines, and microglial activity in brain tissue and cerebrospinal fluid, as well as abnormal peripheral immune cell function. Methods: Adhesion molecules, such as platelet endothelial adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilitate leukocyte transendothelial migration. We assessed concentrations of soluble adhesion molecules, sPECAM-1, sICAM-1, sVCAM-1, sP-selectin, and sL-selectin in the plasma of 49 participants with ASD and 31 typically developing controls of the same age, all of whom were enrolled as part of the Autism Phenome Project. Behavioral assessment, the levels of soluble adhesion molecules, and head circumference were compared in the same subjects. Results: Levels of sPECAM-1 and sP-selectin were significantly reduced in the ASD group compared to typically developing controls (p <.02). Soluble PECAM-1 levels were negatively associated with repetitive behavior and abnormal brain growth in children with ASD (p =.03). Conclusions: Because adhesion molecules modulate the permeability and signaling at the blood-brain barrier as well as leukocyte infiltration into the central nervous system, the current data suggest a role for these molecules in the complex pathophysiology of ASD.
AB - Background: Although the etiopathology of autism spectrum disorder (ASD) is not clear, there is increasing evidence that dysfunction in the immune system affects many children with ASD. Findings of immune dysfunction in ASD include increases in inflammatory cytokines, chemokines, and microglial activity in brain tissue and cerebrospinal fluid, as well as abnormal peripheral immune cell function. Methods: Adhesion molecules, such as platelet endothelial adhesion molecule-1 (PECAM-1), intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), P-selectin, and L-selectin, function to facilitate leukocyte transendothelial migration. We assessed concentrations of soluble adhesion molecules, sPECAM-1, sICAM-1, sVCAM-1, sP-selectin, and sL-selectin in the plasma of 49 participants with ASD and 31 typically developing controls of the same age, all of whom were enrolled as part of the Autism Phenome Project. Behavioral assessment, the levels of soluble adhesion molecules, and head circumference were compared in the same subjects. Results: Levels of sPECAM-1 and sP-selectin were significantly reduced in the ASD group compared to typically developing controls (p <.02). Soluble PECAM-1 levels were negatively associated with repetitive behavior and abnormal brain growth in children with ASD (p =.03). Conclusions: Because adhesion molecules modulate the permeability and signaling at the blood-brain barrier as well as leukocyte infiltration into the central nervous system, the current data suggest a role for these molecules in the complex pathophysiology of ASD.
KW - Adhesion
KW - autism
KW - CD31
KW - CD62-P
KW - P-Selectin
KW - PECAM-1
UR - http://www.scopus.com/inward/record.url?scp=84869082809&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84869082809&partnerID=8YFLogxK
U2 - 10.1016/j.biopsych.2012.05.004
DO - 10.1016/j.biopsych.2012.05.004
M3 - Article
C2 - 22717029
AN - SCOPUS:84869082809
VL - 72
SP - 1020
EP - 1025
JO - Biological Psychiatry
JF - Biological Psychiatry
SN - 0006-3223
IS - 12
ER -