066 – Helminth-Induced Modulation of Neuroinflammation

Printed Poster | Session 1

066 – Helminth-Induced Modulation of Neuroinflammation

Naomi Fettig (1) – Lisa Osborne (1) – Marc Horwitz (1)
University of British Columbia, Microbiology and Immunology, Vancouver, Canada (1)


Multiple sclerosis (MS) is a chronic neurodegenerative disease, in which lymphocyte infiltration into the central nervous system (CNS) induces inflammation, destruction of the myelin sheath, and eventual axonal degradation. MS is caused by both genetic and environmental factors, although the exact environmental factors and their relative contributions to disease progression remain unknown. Epidemiological data show a negative correlation between MS incidence and the prevalence of helminth infections; consequently it has been suggested that helminth infection may offer protection from neuroinflammatory disease, although the mechanism of this interaction remains unknown. One helminth, Trichinella spiralis (Ts) establishes chronic infection by forming nurse cells in the striated muscle and inducing Th2 and regulatory T cell responses, which have been suggested to be protective in MS and in the animal model experimental autoimmune encephalomyelitis (EAE). C57Bl/6 mice were infected with 500 Ts larvae by oral gavage and allowed 4 weeks to establish chronic infection. The mice were subsequently immunized with MOG35-55/CFA to induce EAE. While this model of EAE normally results in a chronic ascending paralysis, prior infection with Ts resulted in delayed disease onset, as well as a remission of symptoms that is not usually observed in C57Bl/6 EAE. Flow cytometric analysis of brain and spinal cord tissues shows decreased lymphocyte infiltration, which will be confirmed by histological analysis by H&E staining. In Ts-infected EAE, the decrease in lymphocytes present in the CNS is accompanied by a Th2-skew in the infiltrating CD4+ T cells. This Th2-skewed response may be inducing T cell-mediated neuroprotection. The type 2 immune environment may induce other immune cells to adopt regulatory or neuroprotective phenotypes, such as alternatively activated macrophages. Macrophage phenotypes within the CNS and periphery will be evaluated by qPCR to determine the cell types involved in Ts-induced attenuation of neuroinflammation and disease course.