Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis

Abstract

Neurocysticercosis (NCC) is the most severe clinical manifestation of cysticercosis. One of the factors responsible for its symptomatology is the host inflammatory response. Therefore the influence of interleukin 4 (IL-4) on the induction of encephalitis in experimental NCC was evaluated. Methods BALB/c (WT) and BALB/c (IL-4-KO) mice were inoculated intracranially with Taenia crassiceps cysticerci and euthanized at 7, 30, 60 and 90 days later, the encephala removed and histopathologically analyzed. Results The absence of IL-4 induced greater parasitism. In the initial phase of the infection, IL-4-KO showed a lower intensity in the inflammatory infiltration of polimorphonuclear cells in the host-parasite interface and intra-parenquimatous edema. The IL-4-KO animals, in the late phase of the infection, showed lower intensity of ventriculomegaly, encephalitis, and meningitis, and greater survival of the parasites in comparison with the WT animals. Conclusion The absence of IL-4 induced lower inflammatory infiltration, ventriculomegaly and perivasculitis in experimental NCC.

Interrelationship and Sequencing of Interleukins4, 13, 31, and 33 – An Integrated Systematic Review: Dermatological and Multidisciplinary Perspectives

“… 168 In their study, Silva et al found that IL-4 knockout mice with experimentally induced neurocysticercosis had lower cerebral edema, lower inflammatory infiltrates and prolonged survival of the parasites in the brain. 169 This indicates that IL-4 is preferentially expressed in response to infections in an attempt to reduce brain damage, possibly explaining the previous observations that asymptomatic patients from endemic areas exhibit increased production of IL-4 and IL-13.…”

ICAM-1 K469E polymorphism, increased risk of neurocysticercosis occurrence and immunopathological defect

“…The role of immunity of the host for protection against neurocysticercosis is very interesting. The observation by Silva et al 2 on interleukin 4 (IL4) and neurocysticercosis is a good example. Here, we would like to draw more attention to a complex immunological defect that can underline increased risk for neurocysticercosis.…”