Aflatoxin B exposure exacerbates chemokine receptor expression in the BTBR T Itpr3/J Mouse Model, unveiling insights into autism spectrum disorder: A focus on brain and spleen.

OBJECTIVE

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by significant difficulties in social interaction, communication, and repeated stereotypic behaviour. Aflatoxin B (AFB) is the most potent and well-known mycotoxin in various food sources. Despite its propensity to generate significant biochemical and structural changes in human and animal tissues, the influence of AFB on ASD has yet to be thoroughly studied. Mounting evidence indicates that chemokine receptors play a crucial function in the central nervous system and are implicated in developing several neuroinflammatory disorders. Chemokine receptors in individuals with ASD were elevated in the anterior cingulate gyrus astrocytes, cerebellum, and brain.

METHODS

The BTBR TItpr3J (BTBR) mice are inbred strains that exhibit strong and consistently observed deficits in social interactions, characterized by excessive self-grooming and limited vocalization in social contexts. We examined the impact of AFB on CCR3-, CCR7-, CCR9-, CXCR3-, CXCR4-, and CXCR6-expressing I-A/I-E cells in the spleen of the BTBR mouse model of autism. We evaluated the mRNA levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 chemokine receptors in the brain.

RESULTS

The exposure to AFB in BTBR mice resulted in a significant rise in the number of I-A/I-ECCR3, I-A/I-ECCR7, I-A/I-ECCR9, I-A/I-ECXCR3, I-A/I-ECXCR4, and I-A/I-ECXCR6 cells. Furthermore, exposure to AFB increased mRNA expression levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 in the brain.

CONCLUSIONS

These findings highlight that AFB exposure increases the expression of chemokine receptors in BTBR mice, indicating the necessity for further research into AFB's role in the development of ASD.