Research Topic

Neurotropism of Parasites and Immune Responses

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Parasitic infections of the central and peripheral nervous systems represent a significant source of morbidity and mortality, especially in humans living in low-to-middle income endemic countries. In spite of the known association between parasitic infections and specific neurological, cognitive and mental ...

Parasitic infections of the central and peripheral nervous systems represent a significant source of morbidity and mortality, especially in humans living in low-to-middle income endemic countries. In spite of the known association between parasitic infections and specific neurological, cognitive and mental disorders, the exact mechanisms by which “neurotropic” parasites (i) enter the central nervous system (CNS) via the blood brain barrier and via the blood CSF barrier and (ii) induce neurological damage have not been fully elucidated yet.

The study of parasitic brain infections is intertwined with that of neuroinflammation and brain damage. A primary role of neuroinflammation is to protect the CNS from insults, including invasion and attack by infectious agents. Pathogens can benefit from immune responses to promote neuroinvasion, for example, when neuroinflammation facilitates the opening of physical barriers, or when the pathogen develops Trojan horse strategies by using activated cells to enter the brain. Once inside the brain, pathogens are difficult to dislodge and cause CNS dysfunctions. This is the case for various protozoan parasites including the intracellular Toxoplasma and the extracellular African trypanosomes. Other pathogens, such as Plasmodium, cause severe alterations and inflammation in the brain vasculature, without entering the brain parenchyma. Metazoan parasites have also evolved mechanisms for invading cerebrospinal tissues. They may invade the CNS via hematogenous spread of larval stages to small vessels, by in situ deposition or embolism of eggs following anomalous migration of adult worms to the CNS, attaching to the nasal neuroepithelium and penetration via the olfactory nerve pathway, or directly invading the neural skull and intervertebral foramina. Parasitic infections also affect the peripheral nervous system (PNS), probably via the production of parasitic molecules (such as cysteine proteases from Entamoeba) and/or via the immune responses stimulated by the infection. The altered activity of peripheral neurons in these infections, through gut-brain communication may modulate immune activity. Distress in the enteric nervous system plays a key role in the pathophysiology of diarrhoea upon exposure to several enteric protozoan and metazoan parasitic infections (i.e. Giardia. sp; E. histolytica). This distress has also been indicated to play a role in chagasic megasyndromes and post-infectious complications.

The roles of systemic innate and adaptive immune responses in the perpetuation or eradication of parasitic infections in the brain is interconnected with the pathogenesis of parasitosis. Understanding these roles will help advance the development of preventive measures against parasite-induced neurological diseases. The purpose of this Research Topic is to cover recent advances in (i) the pathogenesis of parasites affecting the CNS and the PNS, (ii) the role of the immune responses in these infections and (iii) prospects for potential interventions. We welcome the submission of Review, Mini-Review, Opinion and Original Research articles from researchers with expertise in innate and adaptive immunity and neurotropic parasites that cover the following topics:

1. Role of innate and adaptive immune cells in inflammatory processes associated with neuroparasitosis.
2. Pathogenetic mechanisms in CNS and PNS parasitic infections.
3. Interactions between immune cells, parasites and/or parasite-infected cells with the BBB or BCSFB during infection.
4. Mechanisms and regulation of parasite brain invasion.


Keywords: neuroparasitosis, neuroinflammation, innate and adaptive immune cells, BBB, BCSFB, blood brain barrier, brain, CNS infection


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