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DOI 10.1016/j.jneuroim.2023.578253

Медицинская библиотека · Journal of neuroimmunology · 2023

Cadmium exposure exacerbates immunological abnormalities in a BTBR T+ Itpr3tf/J autistic mouse model by upregulating inflammatory mediators in CD45R-expressing cells.

Albekairi Thamer H, Alanazi Mohammed M, Ansari Mushtaq A, Nadeem Ahmed, Attia Sabry M, Bakheet Saleh A, Al-Mazroua Haneen A, Aldossari Abdullah A, Almanaa Taghreed N, Alwetaid Mohammad Y, Alqinyah Mohammed, Alnefaie Hajar O, Ahmad Sheikh F

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

Autism spectrum disorder (ASD) is a neurodevelopmental illness characterized by behavior, learning, communication, and social interaction abnormalities in various situations. Individuals with impairments usually exhibit restricted and repetitive actions. The actual cause of ASD is yet unknown. It is believed, however, that a mix of genetic and environmental factors may play a role in its development. Certain metals have been linked to the development of neurological diseases, and the prevalence of ASD has shown a positive association with industrialization. Cadmium chloride (Cd) is a neurotoxic chemical linked to cognitive impairment, tremors, and neurodegenerative diseases. The BTBR T+ Itpr3tf/J (BTBR) inbred mice are generally used as a model for ASD and display a range of autistic phenotypes. We looked at how Cd exposure affected the signaling of inflammatory mediators in CD45R-expressing cells in the BTBR mouse model of ASD. In this study, we looked at how Cd affected the expression of numerous markers in the spleen, including IFN-γ, IL-6, NF-κB p65, GM-CSF, iNOS, MCP-1, and Notch1. Furthermore, we investigated the effect of Cd exposure on the expression levels of numerous mRNA molecules in brain tissue, including IFN-γ, IL-6, NF-κB p65, GM-CSF, iNOS, MCP-1, and Notch1. The RT-PCR technique was used for this analysis. Cd exposure increased the number of CD45R+IFN-γ+, CD45R+IL-6+, CD45R+NF-κB p65+, CD45R+GM-CSF+, CD45R+GM-CSF+, CD45R+iNOS+, and CD45R+Notch1+ cells in the spleen of BTBR mice. Cd treatment also enhanced mRNA expression in brain tissue for IFN-γ, IL-6, NF-κB, GM-CSF, iNOS, MCP-1, and Notch1. In general, Cd increases the signaling of inflammatory mediators in BTBR mice. This study is the first to show that Cd exposure causes immune function dysregulation in the BTBR ASD mouse model. As a result, our study supports the role of Cd exposure in the development of ASD.

Для цитирования: Albekairi Thamer H, Alanazi Mohammed M, Ansari Mushtaq A, Nadeem Ahmed, Attia Sabry M, Bakheet Saleh A, Al-Mazroua Haneen A, Aldossari Abdullah A, Almanaa Taghreed N, Alwetaid Mohammad Y, Alqinyah Mohammed, Alnefaie Hajar O, Ahmad Sheikh F. Cadmium exposure exacerbates immunological abnormalities in a BTBR T+ Itpr3tf/J autistic mouse model by upregulating inflammatory mediators in CD45R-expressing cells.. Journal of neuroimmunology. 2023. DOI: 10.1016/j.jneuroim.2023.578253.

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