Immunopathology in Taenia solium neurocysticercosis

Abstract

Neurocysticercosis is a clinically and radiologically heterogeneous disease, ranging from asymptomatic infection to a severe, potentially fatal clinical picture. The intensity and extension of the parasite-elicited inflammatory reaction is a key factor for such variability. The main features of the inflammatory process found in the brain and in the peripheral blood of neurocysticercosis patients will be discussed in this review, and the factors involved in its modulation will be herein presented.

Granulomatous responses in larval taeniid infections

“…A finer but important aspect of the picture is that the epithelioid granuloma and the eosinophil‐mediated attack are 2 independently regulated response components that can therefore be present separately or together. Thus, although in T. solium cysticercosis in pigs the 2 components appear to follow parallel courses in muscle sites, brain lesions display granulomas without eosinophil infiltration, and the same happens in human NCC . Immunization of pigs, however, does push the system into eosinophil‐mediated parasite destruction even in the brain .…”

“…Human NCC lesions are classified as “vesicular” (the parasite is morphologically intact and surrounded by scant inflammation), “colloidal” (the parasite is in the process of degeneration and surrounded by strong inflammation), “granular” (the parasite is destroyed and also surrounded by inflammation) and “calcified” . The general consensus is that the live parasite controls local inflammation, and in this situation, neurological symptoms are rare, whereas once the parasite dies, inflammation runs uncontrolled, causing seizures and other neurological symptoms.…”

“…The third point is clear from observations in all systems discussed, and it is probably underpinned by a bidirectional relationship: inflammation causes parasite death, and parasite death causes inflammation. Inflammatory exacerbation following parasite death is a well‐documented phenomenon in NCC and pig models of NCC, including the context of anti‐helminthic pharmacological intervention . Such inflammation is surely the combined result of release of sequestered parasite molecules that constitute danger signals for innate immunity and the discontinuation of parasite‐derived anti‐inflammatory signals.…”

Taenia solium cysticercosis and taeniosis: Achievements from the past 10 years and the way forward

“…Indeed, NCC diagnosis relies on brain imaging which is often unavailable to populations living in endemic areas. However, biomarkers for parenchymal NCC are being discussed and developed [14, 15] while new fusion techniques for combining CT and MRI images are being suggested for better visualization of NCC lesions [16]. …”

“…Viable cysticerci has been shown to provoke a downregulation of inflammatory Th1 response and a switch to Th2 cytokines associated with asymptomatic disease, while a Th1 host response predominantly follows the degeneration of the cysts [15]. Cytokines, other immune mediators and enzymes are important in driving the pro-inflammatory response and increased permeability of the blood brain barrier.…”