Correlation analysis of expression of CC and CXC chemokines in children with autism spectrum disorder

Peng, Guangyang; Peng, Xiaofei; Tong, Tingting; Zhang, Xiuyun; Xu, Min; Peng, Xiaofang

doi:10.1097/md.0000000000026391

Cited by 7 publications

(2 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, proin ammatory cytokines and chemotactic factors, such as TNF-α, IL-6, MCP-1 and IL-17, are also thought to take part in the disruption of the BBB, giving rise to 'focal encephalitis' in speci c brain areas [38][39][40][41][42]. Many studies have reported notably higher levels of TNF-α, IL-6 and MCP-1 in the periphery of ASD patients and autism-like rodent animal models [32][33][43][44]. The mRNA levels of TNF-, IL-6 and MCP-1 were signi cantly higher in the cortex of newborn BTBR mice than in C57BL/6 mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

Early postnatal activation of A2ARs alleviates social deficits by attenuating the abnormal infiltration of peripheral neutrophils in the BTBR T + Itpr3 tf /J mouse model of autism

Zhou

Yang

et al. 2022

Preprint

View full text Add to dashboard Cite

Background Previous studies have mainly focused on the immediate effect of drugs on autism spectrum disorders (ASDs) and complex heterogeneous neurodevelopmental disorders that have been proven to be involved with the chronic inflammation of the central nervous system. Our prior work has explored the positive role of activation of adenosine 2A receptors (A2ARs) in protecting adult BTBR T+ Itpr3tf/J mice against autism-related behaviour from the early postnatal period. However, the exact mechanism underlying the protection of A2ARs has not been comprehensively investigated. Methods The persistent protection of early postnatal activation of A2ARs in adult BTBR mice was detected utilizing behaviour tests. Pathological variation in the peripheral blood of autism patients was analysed by transcriptomic analysis, including MROAST and protein–protein interaction (PPI) analysis. The clues were further explored and validated by real-time (RT) PCR, western blotting, immunohistochemistry and transcriptomic analysis in the mouse cortex. The blood brain barrier of mice was identified by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). Results Abnormal activation of myeloid cells, especially neutrophils, was detected in the peripheral blood of autism patients and the BTBR mouse cortex. The BBB permeability of BTBR mice was significantly increased, which may have facilitated the abnormal infiltration of neutrophils observed in the BTBR mouse cortex. Furthermore, the early postnatal activation of A2ARs effectively reverses the abnormal activation and invasion of neutrophils in the mouse cortex and might result in the significant moderation of autism-related behaviour in adult BTBR mice, followed by a decrease in chronic inflammation in the mouse cortex during the early postnatal period. Conclusions We found abnormal myeloid cells in autism patients and BTBR mice and increased infiltration of neutrophils in the mouse cortex. We concluded that the early activation of A2ARs could effectively decrease the autism-related behaviour of adult BTBR mice by reversing the abnormal activation of myeloid cells and the pathological invasion of neutrophils in the mouse cortex.

show abstract

Section: Discussionmentioning

confidence: 99%

Early postnatal activation of A2ARs alleviates social deficits by attenuating the abnormal infiltration of peripheral neutrophils in the BTBR T + Itpr3 tf /J mouse model of autism

Zhou

Yang

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Besides, pro-in ammatory cytokines and chemotactic factors, TNF-α, IL-6, MCP-1 and IL-17 for example, are also considered to take part in the disruption of BBB which have given rise to 'focal encephalitis' in speci c brain areas [38][39][40][41][42]. Ample of studies have reported the notably rising levels of TNF-α, IL-6 and MCP-1 in the periphery of ASDs patients and the autism like rodent animal models [32][33][43][44]. It was identi ed that the mRNA level of TNF-, IL-6 and MCP-1 were signi cantly higher in the cortex of newborn BTBR mice than in C57BL/6 mice as well (Fig.…”

Section: Discussionmentioning

confidence: 99%

The early postnatal activation of A2ARs protects BTBR mice against autism related behavior

Zhou

Yang

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: Studies mainly focused on the immediate effect of drugs on Autism spectrum disorders (ASD), the complex heterogeneous neurodevelopmental disorders, which been proved involved with the chronic inflammation of the central nervous system. Our studies have explored the positive role of activation of adenosine 2A receptors (A2ARs) in protect adult BTBR mice against autism related behavior from the early postnatal period. However, the exact mechanism underlying the protection of A2ARs has not been comprehensively investigated. Methods: The persistent protection of early postnatal activation of A2ARs in the adult BTBR mice were detected utilizing behavior tests. Pathological variation in the peripheral blood of autism patients were analyzed by transcriptomic analysis, including mroast and protein–protein interactions (PPIs). The clues were further explored and validated by real-time RT PCR, western blotting, immunohistochemistry and transcriptomic analysis in the mouse cortex. The blood brain barrier of mouse were spotted by dynamic contrast enhanced magnetic resonance imaging (DCE-MRI). Results: Abnormal activation of myeloid cells, especially the neutrophil were detected in the peripheral blood of autism patients and BTBR mouse cortex. The BBB permeability of BTBR mouse were significantly increased, which might facilitated the abnormal infiltration of neutrophils spotted in the BTBR mouse cortex. Further, the early postnatal activation of A2ARs effectively revers the abnormal activation and invading of neutrophils in the mouse cortex, might result in the significantly moderation of the autism related behavior of adult BTBR mice, following decrease of the chronic inflammation in the mouse cortex during the early postnatal period. Conclusions: We found the abnormal condition of myeloid cells in the autism patients and BTBR mice, and the adding infiltration of neutrohpils in the mouse cortex. We concluded that the early activation of A2ARs could effectively decreased the autism related behavior of adult BTBR mice via reversing the abnormal activation of myeloid cells and the pathological invading of neutrophils in the mouse cortex.

show abstract

Prenatal Programming of Monocyte Chemotactic Protein-1 Signaling in Autism Susceptibility

Camacho-Morales,

Cárdenas-Tueme

2024

Mol Neurobiol

View full text Add to dashboard Cite

Correlation analysis of expression of CC and CXC chemokines in children with autism spectrum disorder

Cited by 7 publications

References 20 publications

Early postnatal activation of A2ARs alleviates social deficits by attenuating the abnormal infiltration of peripheral neutrophils in the BTBR T + Itpr3 tf /J mouse model of autism

Early postnatal activation of A2ARs alleviates social deficits by attenuating the abnormal infiltration of peripheral neutrophils in the BTBR T + Itpr3 tf /J mouse model of autism

The early postnatal activation of A2ARs protects BTBR mice against autism related behavior

Prenatal Programming of Monocyte Chemotactic Protein-1 Signaling in Autism Susceptibility

Contact Info

Product

Resources

About