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

• Published in: Journal of neuroinflammation Vol. 8; no. 1; p. 180
• Main Authors: Mostafa, Gehan A, Al-Ayadhi, Laila Y
• Format: Journal Article
• Language: English
• Published: England BioMed Central 21.12.2011; BioMed Central Ltd; BMC
• Subjects: Anti-ribosomal P protein antibodies; autism; Autistic Disorder - blood; Autistic Disorder - immunology; Autoantibodies - blood; Autoantibodies - immunology; Autoimmune diseases; autoimmunity; Child; Cross-Sectional Studies; Female; Humans; Immune system; Male; Medical research; neurokinin A; Neurokinin A - blood; Proteins; Ribosomal Proteins - immunology; Rodents; Saudi Arabia; Saudi Arabia
• ISSN: 1742-2094; 1742-2094
• DOI: 10.1186/1742-2094-8-180

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. Serum neurokinin A and anti-ribosomal P protein antibodies were measured in 70 autistic children in comparison to 48 healthy-matched children. 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). 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.