Prof. Dr. Vladimir Trajkovski

srijeda, 18.07.2012.

Corticotropin-releasing hormone and extracellular mitochondria augment IgE-stimulated human mast-cell vascular endothelial growth factor release, which is inhibited by luteolin.

J Neuroinflammation. 2012 May 4;9(1):85. [Epub ahead of print]

Corticotropin-releasing
hormone and extracellular mitochondria augment IgE-stimulated human
mast-cell vascular endothelial growth factor release, which is inhibited
by luteolin.



Asadi S, Theoharides TC.


Abstract



BACKGROUND:


Autism
Spectrum Disorders (ASD) are neurodevelopmental disorders characterized
by varying degrees of dysfunctional social abilities, as well as
learning deficits, and stereotypic behaviors. Many ASD patients have
"allergic like" symptoms and respond disproportionally to stress. We had
shown that the peptide neurotensin (NT) is increased in the serum of
young autistic children and that can stimulate extracellular secretion
of mitochondrial (mt) DNA (mtDNA), which was also increasesd in the
serum of these children.

METHODS:


Human mast cells were
stimulated by corticotropin-releasing hormone (CRH), mt, IgE/anti-IgE
for either 24 h for measuring vascular endothelial growth factor (VEGF)
release by ELISA or 6 h for qPCR.

RESULTS:


Here we show
that CRH augments IgE/anti-IgE-induced human mast cell release of VEGF
and that it also induces the expression of IgE receptor (FcepsilonRI) on
mast cells. Moreover, we show that sonicated mt also augment VEGF
release, and that this effect is blocked by the natural flavone
luteolin.

CONCLUSION:


These results indicate that stress
and infection-mimicking extracellular mt components augment allergic
inflammation that may be involved in the early pathogenesis of ASD.
Moreover, luteolin inhibits these processes and may be helpful in the
treatment of ASD.


PMID:22559745
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