Gut Pathogens and Cytokine Profiles in Autism: A Multi-Biosample Analysis.

Researchers compared blood, saliva, and stool samples from 20 children with autism to 10 children without autism in Iraq. They found much higher levels of inflammation markers in the autism group's blood. The gut bacteria were also different, with more harmful bacteria found in children with autism. These inflammation markers might help doctors diagnose autism earlier, but more research is needed.

This cross-sectional study examined immune, microbial, and gene expression differences between 20 Iraqi children with ASD and 10 healthy controls using blood, saliva, and stool samples. Results showed significantly elevated pro-inflammatory cytokines in ASD participants: IL-1β (2275.9 vs 429.3 pg/mL), IL-6 (109.9 vs 47.6 pg/mL), IL-17A (1457.7 vs 963.6 pg/mL), and TNF-α (367.2 vs 148.8 pg/mL). Gene expression patterns mirrored serum findings. Stool analysis revealed predominant Escherichia species, including pathogenic strains.

ROC analysis indicated excellent diagnostic potential for cytokine markers. The study suggests ASD may be characterized by systemic inflammation and gut microbial dysbiosis, with IL-6 and TNF-α showing promise as biomarkers.

Findings suggest potential for cytokine-based biomarkers in ASD diagnosis and monitoring. Results support investigating anti-inflammatory interventions and gut microbiome therapies. However, larger multi-center studies needed before clinical implementation. Current findings warrant replication across diverse populations.

Small sample size (n=30) limits generalizability. Single-center study from specific population (Iraqi). Cross-sectional design cannot establish causation. ROC analysis results not fully detailed. No correction for multiple comparisons reported. Study type not specified.

To explore immune, microbial, and gene expression alterations in children with autism spectrum disorder (ASD), assessing their potential as diagnostic markers. Thirty participants, 20 with ASD (15 male, 5 female) and 10 healthy controls, underwent collection of saliva, blood, and stool. Serum cytokines (IL-1β, IL-6, IL-17A, TNF-α) were quantified via ELISA. RT-qPCR assessed corresponding gene expression in blood and saliva.

Stool cultures yielded bacterial isolates identified by 16S rRNA sequencing methods. Diagnostic accuracy of cytokines was evaluated using ROC curves. Familial history revealed Down syndrome in 25% of ASD families. Stool cultures produced 31 isolates, predominantly Escherichia (23 E. coli, 5 E. fergusonii, including enterohemorrhagic strains).

ASD patients exhibited significantly higher serum cytokine levels (mean ± SE, pg/mL): IL-1β 2275.9 versus 429.3; IL-6109.9 versus 47.6; IL-17A 1457.7 versus 963.6; TNF-α 367.2 versus 148.8 (p < 0.01). Cytokines were strongly intercorrelated, and ROC analysis showed excellent diagnostic potential. Gene expression mirrored serum findings, while salivary cytokine expression varied. Cytokine expression correlated closely with serum protein levels.

ASD in this Iraqi cohort is characterized by strong pro-inflammatory signatures and microbial dysbiosis, with IL-6 and TNF-α emerging as potential biomarkers. These markers warrant further investigation for early diagnosis and targeted interventions.