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The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism

BACKGROUND: Neurogenic inflammation is orchestrated by a large number of neuropeptides. Tachykinins (substance P, neurokinin A and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases. Autoimmunity may have a role in the patho...

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Autores principales: Mostafa, Gehan A, AL-Ayadhi, Laila Y
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261830/
https://www.ncbi.nlm.nih.gov/pubmed/22189180
http://dx.doi.org/10.1186/1742-2094-8-180
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author Mostafa, Gehan A
AL-Ayadhi, Laila Y
author_facet Mostafa, Gehan A
AL-Ayadhi, Laila Y
author_sort Mostafa, Gehan A
collection PubMed
description BACKGROUND: Neurogenic inflammation is orchestrated by a large number of neuropeptides. Tachykinins (substance P, neurokinin A and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases. Autoimmunity may have a role in the pathogenesis of autism in some patients. We are the first to measure serum neurokinin A levels in autistic children. The relationship between serum levels of neurokinin A and anti-ribosomal P protein antibodies was also studied. METHODS: Serum neurokinin A and anti-ribosomal P protein antibodies were measured in 70 autistic children in comparison to 48 healthy-matched children. RESULTS: Autistic children had significantly higher serum neurokinin A levels than healthy controls (P < 0.001). Children with severe autism had significantly higher serum neurokinin A levels than patients with mild to moderate autism (P < 0.001). Increased serum levels of neurokinin A and anti-ribosomal P protein antibodies were found in 57.1% and 44.3%, respectively of autistic children. There was significant positive correlations between serum levels of neurokinin A and anti-ribosomal P protein antibodies (P = 0.004). CONCLUSIONS: Serum neurokinin A levels were elevated in some autistic children and they were significantly correlated to the severity of autism and to serum levels of anti-ribosomal P protein antibodies. However, this is an initial report that warrants further research to determine the pathogenic role of neurokinin A and its possible link to autoimmunity in autism. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, should also be studied in autism.
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spelling pubmed-32618302012-01-20 The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism Mostafa, Gehan A AL-Ayadhi, Laila Y J Neuroinflammation Research BACKGROUND: Neurogenic inflammation is orchestrated by a large number of neuropeptides. Tachykinins (substance P, neurokinin A and neurokinin B) are pro-inflammatory neuropeptides that may play an important role in some autoimmune neuroinflammatory diseases. Autoimmunity may have a role in the pathogenesis of autism in some patients. We are the first to measure serum neurokinin A levels in autistic children. The relationship between serum levels of neurokinin A and anti-ribosomal P protein antibodies was also studied. METHODS: Serum neurokinin A and anti-ribosomal P protein antibodies were measured in 70 autistic children in comparison to 48 healthy-matched children. RESULTS: Autistic children had significantly higher serum neurokinin A levels than healthy controls (P < 0.001). Children with severe autism had significantly higher serum neurokinin A levels than patients with mild to moderate autism (P < 0.001). Increased serum levels of neurokinin A and anti-ribosomal P protein antibodies were found in 57.1% and 44.3%, respectively of autistic children. There was significant positive correlations between serum levels of neurokinin A and anti-ribosomal P protein antibodies (P = 0.004). CONCLUSIONS: Serum neurokinin A levels were elevated in some autistic children and they were significantly correlated to the severity of autism and to serum levels of anti-ribosomal P protein antibodies. However, this is an initial report that warrants further research to determine the pathogenic role of neurokinin A and its possible link to autoimmunity in autism. The therapeutic role of tachykinin receptor antagonists, a potential new class of anti-inflammatory medications, should also be studied in autism. BioMed Central 2011-12-21 /pmc/articles/PMC3261830/ /pubmed/22189180 http://dx.doi.org/10.1186/1742-2094-8-180 Text en Copyright ©2011 Mostafa and AL-Ayadhi; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Mostafa, Gehan A
AL-Ayadhi, Laila Y
The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title_full The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title_fullStr The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title_full_unstemmed The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title_short The possible link between the elevated serum levels of neurokinin A and anti-ribosomal P protein antibodies in children with autism
title_sort possible link between the elevated serum levels of neurokinin a and anti-ribosomal p protein antibodies in children with autism
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3261830/
https://www.ncbi.nlm.nih.gov/pubmed/22189180
http://dx.doi.org/10.1186/1742-2094-8-180
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