β-Glucan alleviates goal-directed behavioral deficits in mice infected with Toxoplasma gondii

• Published in: Parasites & vectors Vol. 16; no. 1; pp. 65 - 15
• Main Authors: Cui, Zeyu, Gong, Yuying, Luo, Xiaotong, Zheng, Niuyi, Tan, Shimin, Liu, Shuxi, Li, Youwei, Wang, Qingling, Sun, Fenfen, Hu, Minmin, Pan, Wei, Yang, Xiaoying
• Format: Journal Article
• Language: English
• Published: England BioMed Central 13-02-2023; BMC
• Subjects: Alzheimer's disease; Animal cognition; Animals; Astrocytes; Axons; Behavior disorders; beta-Glucans; Chronic infection; Cognitive ability; Cognitive impairment; Cysts; Cytokines; Degeneration; Disorders; Drug development; Electron microscopy; Glucan; Goals; Immunity; Immunofluorescence; Impairment; Infections; Inflammation; Injury prevention; Invasiveness; Medical research; Memory; Mice; Microglia; Neuroinflammation; Neuroinflammatory Diseases; Neuroprotection; Nucleotide sequence; Parasites; Parkinson's disease; Prefrontal cortex; Protozoa; Risk taking; Temporal lobe; Temporal variations; Toxoplasma; Toxoplasma gondii; Toxoplasma gondii; Toxoplasmosis - parasitology; Transmission electron microscopy; Ultrastructure; β-Glucan; United States > US; China; Neuroinflammation; Prefrontal cortex; β-Glucan; Toxoplasma gondii; Cognitive impairment
• ISSN: 1756-3305; 1756-3305
• DOI: 10.1186/s13071-023-05686-4

Toxoplasma gondii (T. gondii) is a neuroinvasive parasite causing neuroinflammation, which in turn 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. 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. gondii infection 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.
A mice model of chronic T. gondii Wh6 infection was established by infecting mice by oral gavage with 10 cysts of T. gondii Wh6. Intraperitoneal injection of β-glucan was manipulated 2 weeks before T. gondii infection. Performance of the infected mice on the Y-maze test and temporal order memory (TOM) test was used 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.
The administration of β-glucan significantly prevented T. gondii Wh6-induced goal-directed behavioral impairment as assessed behaviorally by the Y-maze test and TOM test. In the prefrontal cortex, β-glucan was able to 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.
This study revealed that β-glucan prevents goal-directed behavioral impairment induced by chronic T. gondii infection in mice. These findings suggest that β-glucan may be an effective drug candidate to prevent T. gondii-associated psycho-behavioral disorders including goal-directed behavioral injury.