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Altered Stool Cytokine Profiles and Pro-Inflammatory/Anti-Inflammatory Imbalance in Children with Autism Spectrum
Petra Finderle1,2, Maja Jekovec Vrhovšek3, Uršula Prosenc Zmrzljak4
1Institute of Clinical Chemistry and Biochemistry, University Medical Centre Ljubljana, Zaloška cesta 2, 1000 Ljubljana, Slovenia.
Children with autism spectrum disorder (ASD) exhibit lower levels of stool IL-8 and IL-4, indicating immune dysregulation, particularly in early childhood. This study highlights a potential developmental window for gut inflammation in ASD.
Area of Science:
- Immunology
- Neuroscience
- Gastroenterology
Background:
- Immune dysregulation and gut dysbiosis are increasingly linked to autism spectrum disorder (ASD).
- Compartment-specific intestinal cytokine profiles in ASD remain poorly understood.
- Understanding these profiles is crucial for identifying potential therapeutic targets.
Purpose of the Study:
- To characterize stool cytokine profiles in children with ASD.
- To analyze the pro-inflammatory and anti-inflammatory balance in the gut of children with ASD.
- To examine how these profiles change across different developmental stages in ASD.
Main Methods:
- Analyzed stool samples from 283 children (109 controls, 104 mild ASD, 70 severe ASD) aged 0.9-21.5 years.
- Measured nine cytokines (IFN-γ, IL-1α, IL-1β, IL-4, IL-6, IL-8, IL-10, IL-17, TNF-α) using Luminex assay.
- Calculated a composite pro-/anti-inflammatory ratio and performed age-stratified analyses.
Main Results:
- Children with ASD showed significantly decreased stool IL-8 and IL-4 compared to controls.
- Reductions in IL-8 were prominent in younger children (≤9.5 years), while IL-1β levels showed a trend reversal with age.
- A higher pro-/anti-inflammatory ratio was observed in severe ASD, especially in older children, with inverse correlations between IL-8/IL-1β and CARS scores.
Conclusions:
- ASD is associated with reduced stool IL-8 and IL-4 and a pro-inflammatory gut cytokine balance, most pronounced in early development.
- Findings support a hypothesis of a developmental window for intestinal immune dysregulation in ASD.
- Further independent replication is needed to draw clinical conclusions.
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