Autism spectrum disorder (ASD) is a severe neurodevelopmental disorder characterized by deficits in social interaction, communication, and repetitive behaviors. A key role for immune dysfunction has been suggested in ASD. Recent studies have indicated that inflammatory mediators and Notch-1 signaling may contribute to the development of ASD. Methylmercury chloride (MeHgCl) is an environmental pollutant that primarily affects the central nervous system, causing neurological alterations. Its effects on immunological responses have not been fully investigated in ASD. In this study, we examined the influence of MeHgCl exposure on inflammatory mediators and Notch-1 signaling in BTBR T⁺ Itpr3tf/J (BTBR) mice, a model of ASD. We examined the effects of MeHgCl on the IL-6-, GM-CSF-, NF-κB p65-, Notch-1-, and IL-27-producing CD14⁺ and CD40⁺ cells in the spleen. We assessed the effect of MeHgCl on IL-6, GM-CSF, NF-κB p65, Notch-1, and IL-27 mRNA levels in brain tissue. We also measured IL-6, GM-CSF, and NF-κB p65 protein expression levels in brain tissue. MeHgCl exposure of BTBR mice significantly increased IL-6-, GM-CSF-, NF-κB p65-, and Notch-1-, and decreased IL-27-producing CD14⁺, and CD40⁺ cells in the spleen. MeHgCl exposure of BTBR mice upregulated IL-6, GM-CSF, NF-κB p65, and Notch-1, and decreased IL-27 mRNA expression levels in brain tissue. Moreover, MeHgCl resulted in elevated expression of the IL-6, GM-CSF, and NF-κB p65 proteins in brain tissue. Taken together, these results indicate that MeHgCl exposure aggravates proinflammatory mediators and Notch-1 signaling which are associated with imbalance of neuroimmune function in BTBR mice.

自闭症谱系障碍（ASD）是一种严重的神经发育障碍，其特征是社交、交流和重复行为方面的缺陷。在 ASD 中已经提出了免疫功能障碍的关键作用。最近的研究表明炎症介质和 Notch-1 信号可能有助于 ASD 的发展。甲基氯化汞 (MeHgCl) 是一种环境污染物，主要影响中枢神经系统，导致神经系统改变。尚未在 ASD 中充分研究其对免疫反应的影响。在这项研究中，我们检查了 MeHgCl 暴露对 BTBR T ⁺ Itpr3tf/ J 中炎症介质和 Notch-1 信号传导的影响(BTBR) 小鼠，一种 ASD 模型。我们检查了 MeHgCl 对脾脏中产生 IL-6-、GM-CSF-、NF-κB p65-、Notch-1- 和 IL-27 的 CD14 ⁺和 CD40 ⁺细胞的影响。我们评估了 MeHgCl 对脑组织中 IL-6、GM-CSF、NF-κB p65、Notch-1 和 IL-27 mRNA 水平的影响。我们还测量了脑组织中的 IL-6、GM-CSF 和 NF-κB p65 蛋白表达水平。BTBR 小鼠的 MeHgCl 暴露显着增加了 IL-6-、GM-CSF-、NF-κB p65- 和 Notch-1-，并降低了产生 IL-27 的 CD14 ⁺和 CD40 ⁺脾脏中的细胞。BTBR 小鼠的 MeHgCl 暴露上调了 IL-6、GM-CSF、NF-κB p65 和 Notch-1，并降低了脑组织中 IL-27 mRNA 的表达水平。此外，MeHgCl 导致脑组织中 IL-6、GM-CSF 和 NF-κB p65 蛋白的表达升高。总之，这些结果表明 MeHgCl 暴露会加剧与 BTBR 小鼠神经免疫功能失衡相关的促炎介质和 Notch-1 信号传导。