Parasite infections, neuroinflammation, and potential contributions of gut microbiota

Abstract

Many parasitic diseases (including cerebral malaria, human African trypanosomiasis, cerebral toxoplasmosis, neurocysticercosis and neuroschistosomiasis) feature acute or chronic brain inflammation processes, which are often associated with deregulation of glial cell activity and disruption of the brain blood barrier’s intactness. The inflammatory responses of astrocytes and microglia during parasite infection are strongly influenced by a variety of environmental factors. Although it has recently been shown that the gut microbiota influences the physiology and immunomodulation of the central nervous system in neurodegenerative diseases like Alzheimer’s disease and Parkinson’s, the putative link in parasite-induced neuroinflammatory diseases has not been well characterized. Likewise, the central nervous system can influence the gut microbiota. In parasite infections, the gut microbiota is strongly perturbed and might influence the severity of the central nervous system inflammation response through changes in the production of bacterial metabolites. Here, we review the roles of astrocytes and microglial cells in the neuropathophysiological processes induced by parasite infections and their possible regulation by the gut microbiota.

Specialized Pro-Resolving Lipid Mediators: Endogenous Roles and Pharmacological Activities in Infections

“…For example, eggs and larvae frequently induce granuloma formation and fibrosis, protozoans trigger Th1 response with high levels of IFN-γ and TNF-α, and helminths induce a strong Th2 response with significant eosinophilia [ 168 ]. Furthermore, parasitic infections often feature acute or chronic neuroinflammation and are linked to an assortment of clinical outcomes, as pro-inflammatory cytokines released by microglial cells and astrocytes are key players of the pathological process [ 169 ]. The presence of parasites can impair the activity of glial cells, and this is commonly related with pro-inflammatory mediators’ levels, cytotoxic action of nitric oxide, and reactive oxygen species [ 169 ].…”

“…Furthermore, parasitic infections often feature acute or chronic neuroinflammation and are linked to an assortment of clinical outcomes, as pro-inflammatory cytokines released by microglial cells and astrocytes are key players of the pathological process [ 169 ]. The presence of parasites can impair the activity of glial cells, and this is commonly related with pro-inflammatory mediators’ levels, cytotoxic action of nitric oxide, and reactive oxygen species [ 169 ]. When the infection becomes chronic, persistence of the pathogen leads to tissue damage and perpetuates inflammatory processes, markedly characterized by cellular infiltrate, composed mainly of T cytotoxic and T helper lymphocytes, macrophages, and B cells [ 170 ].…”

Neuroinflammation in Alzheimer’s Disease: A Potential Role of Nose-Picking in Pathogen Entry via the Olfactory System?

“…Several pathogens have been associated with AD, including viruses (e.g., herpes simplex virus type 1-HSV-1), bacteria (e.g., Chlamydia pneumoniae, spirochetes, treponemes) [22][23][24], fungi such as Candida albicans [25], and parasites such as Toxoplasma gondii [26]. These pathogens are known to establish persistent, latent, or chronic infections in peripheral tissues, including the nasal epithelium, where they may persist for extended periods without causing overt symptoms, until they enter the brain with pathological consequences (Figure 1).…”

Neuroinflammatory Part of the Systemic Inflammatory Process in the Development of Neurodegenerative Conditions

“…Наиболее частыми примерами внеклеточных паразитозов являются аскаридозы и описторхозы, протекающие нередко бессимптомно или с преобладающей кишечной симптоматикой. При этом уровень системного воспаления и повреждения печени при глистных инвазиях высок и может проявляться в виде кожных высыпаний, дерматитов, обструктивного синдрома, а при повышении проницаемости гематоэнцефалического барьера и в появлении психоневрологической симптоматики [39][40][41].…”