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REVIEW article
Front. Microbiol.
Sec. Infectious Agents and Disease
Volume 15 - 2024 |
doi: 10.3389/fmicb.2024.1512233
This article is part of the Research Topic Inflammation and toxoplasmosis - immunological and pathological consequences View all articles
Pathological Mechanisms Of Glial Cell Activation And Neurodegenerative And Neuropsychiatric Disorders Caused By Toxoplasma gondii Infection
Provisionally accepted- Southern Medical University, Guangzhou, China
Toxoplasma gondii is an intracellular opportunistic parasite that exists in a latent form within the human central nervous system (CNS), even in immune-competent hosts.During acute infection, T. gondii traverses the blood-brain barrier (BBB). In the subsequent chronic infection phase, the infiltration of immune cells into the brain, driven by T. gondii infection and the formation of parasitic cysts, leads to persistent activation and proliferation of astrocytes and microglia. This process results in neuronal damages that are fatal in some cases. Through inducing systemic immune responses, T. gondii infection can dramatically alter the behavior of rodents and increase the risk of various neuropsychiatric disorders in humans. In this review, we explore some recent research progress on the major events involved in BBB disruption, glial cell activation and neuronal damage following T. gondii infection in hosts. It further discusses potential pathological mechanisms and the feasible treatment approaches for the neurodegenerative and neuropsychiatric disorders caused by T. gondii infection to extend our understanding for pathogenesis and preventive control of toxoplasmosis in humans.
Keywords: Toxoplasma gondii, glial cell activation, neuropsychiatric disorders, Blood-Brain Barrier, neuronal damage
Received: 16 Oct 2024; Accepted: 26 Nov 2024.
Copyright: © 2024 Yang, Chen, Zhang and Peng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hong-Juan Peng, Southern Medical University, Guangzhou, China
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