β-glucan alleviates goal-directed behavior in mice infected with Toxoplasma gondii

Author:

Cui Zeyu1,Gong Yuying2,Luo Xiaotong1,Zheng Niuyi3,Tan Shimin1,Liu Shuxi4,Li Youwei4,Wang Qingling5,Sun Fenfen2,Hu Minmin2,Pan Wei2,Yang Xiaoying Yang2

Affiliation:

1. The Second Clinical Medical College, Xuzhou Medical University, Xuzhou, Jiangsu

2. Jiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogen Biology and Immunology, Xuzhou Medical University, Xuzhou, Jiangsu

3. Department of Anatomy, Basic Medical College, Xuzhou Medical University, Xuzhou, Jiangsu

4. The First Clinical Medical College, Xuzhou Medical University, Xuzhou, Jiangsu

5. Department of pathology, Basic Medical College, Xuzhou Medical University, Xuzhou, Jiangsu

Abstract

Abstract Background Toxoplasma gondii (T. gondii) is a neuroinvasive parasite causing neuroinflammation, which is associated with a higher risk for several psycho-behavioral disorders. There is an urgent need to identify drugs capable of improving cognitive deficits induced by T. gondii infection. (1, 3)/(1, 6)-β-glucan, an active ingredient in mushrooms, could significantly enhance immunity. However, the effects of β-glucan against neuroinflammation and cognitive decline induced by T. gondiiinfection remain unknown. The present study aimed to investigate the neuroprotective effect of β-glucan on goal-directed behavior of mice chronically infected by T. gondii Wh6 strain. Methods A mice model of chronic T. gondii Wh6 infection was established by gavage of 10 cysts. Intraperitoneal injection of β-glucan was manipulated two weeks before T. gondiiinfection. Y-maze test and temporal order memory (TOM) test were performed to assess the goal-directed behavior. Golgi-Cox staining, transmission electron microscopy, immunofluorescence, Real-Time PCR and western blot assays were used to detect prefrontal cortex-associated pathological change and neuroinflammation. Results We reported that administration of β-glucan significantly prevented T. gondii Wh6-induced goal-directed behavioral impairment assessed behaviorally by Y-maze test and TOM test. In the prefrontal cortex, β-glucan could counter T. gondii Wh6 -induced degeneration of neurites, impairment of synaptic ultrastructure, and decrease of pre- and postsynaptic protein levels. Also, β-glucan significantly prevented the hyperactivation of pro-inflammatory microglia and astrocytes, as well as the upregulation of proinflammatory cytokines caused by chronic T. gondii Wh6 infection. Conclusion This study revealed that β-glucan prevents goal-directed behavioral impairment induced by chronic T. gondii infection in mice. These findings suggested that β-glucan may be an effective drug candidate to prevent T. gondii-associated psycho-behavioral disorders including goal-directed behavioral injury.

Publisher

Research Square Platform LLC

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