Epidemiological and experimental studies have indicated that helminth infections can ameliorate autoimmune diseases. The present study investigated the amelioration effect of the Trichinella pseudospiralis infection on experimental autoimmune encephalomyelitis (EAE), a T-cell-mediated autoimmune disease of central nervous system (CNS), and expression kinetics of Th17 and Th1 cytokine which play a crucial role in the pathogenesis of EAE. The results indicated that the infection of helminth T. pseudospiralis obviously ameliorated clinical severity and greatly delayed the onset of EAE induced by myelin oligodendrocyte glycoprotein (MOG) immunization. Infection caused much lesser inflammatory infiltration and demyilination in the CNS of infected EAE mice than uninfected EAE mice. The reduced infiltration was also suggested by the expressions of the inflammation cytokines, IL-17, IL-6, IL-1β, IFN-γ, and TNF-α, which were high in the spinal cords of the uninfected EAE mice, but was nearly normal or low in the infected EAE mice. The increased production of MOG-induced IL-17 and IFN-γ and the expression of IL-6, IL-1β, TGF-β in splenocytes after restimulation with MOG was inhibited in the infected EAE mice. On the other hand, the greatly induced Th2 response was observed in the splenocytes of the infected EAE mice. The present study showed that T. pseudospiralis infection can suppresses EAE by reducing the inflammatory infiltration in CNS, likely associated with the suppression of Th17 and Th1 responses by the infection.

Vertebrate lens tissues contain several species of acidic and neutral glycosphingolipids in relatively high amounts. However, the epithelia with capsule from dog and rhesus monkey lenses had a simpler composition and lower content of glycosphingolipids than whole lenses. Gangliosides and neutral glycosphingolipids in monolayer cultures of lens epithelial cells were also different from those in whole lenses. Although alpha-galactosyl (Gal alpha 1-3Gal-R) or Lewis(x) (Gal beta 1-4[Fuc alpha 1-3]GlcNAc-R) epitopes were found in glycosphingolipids from whole lenses, they were not detected in those from monolayer cultures of dog and rhesus monkey lens cells. In addition, significant changes in ganglio-series gangliosides were induced in monolayer cultures of both cells, where GM3 and GD3 were predominant. Immunofluorescence study revealed a characteristic distribution of cell surface gangliosides in confluent monolayers. These findings suggest that glycosphingolipid synthesis in lens epithelia is intrinsically different from that in cortical and nuclear fibres, and that the expression of Lewis(x) and alpha-galactosyl epitopes in glycosphingolipids appears to be associated with the differentiation of epithelial cells to fibres.

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cInfectious microorganisms often modify host immunity to escape from immune elimination. Trichinella is a unique nematode of the helminth family, whose members parasitize the muscle cells inside the host without robust eliminative reactions. There are several species of Trichinella; some develop in muscle cells that become encapsulated (e.g., Trichinella spiralis) and others in cells that do not encapsulate (e.g., Trichinella pseudospiralis). It has already been established that Trichinella infection affects host immune responses in several experimental immune diseases in animal models; however, most of those studies were done using T. spiralis infection. As host immune responses to T. spiralis and T. pseudospiralis infections have been reported to be different, it is necessary to clarify how T. pseudospiralis infection influences the host immune responses. In this study, we investigated the influence on host humoral immunity in T. pseudospiralis-infected mice. We demonstrated that T. pseudospiralis infection decreased antigen-specific IgG2a and IgG2b antibody (Ab) production in mice immunized with a model antigen. This selective decrease in gamma interferon (IFN-␥)-dependent Ab production was not due to a decrease in IFN-␥ production, and we instead found impaired follicular helper T (Tfh) cell differentiation. The affinity maturation of antigen-specific Ab tended to be delayed but was not significant in T. pseudospiralis-infected mice. We also observed that CD11b ؉ spleen cells in T. pseudospiralis-infected mice expressed CD206 and PD-L2, the phenotype of which was M2 macrophages with weak production of interleukin-6 (IL-6), possibly resulting in impaired Tfh differentiation. Taken together, our results indicate that nonencapsulated Trichinella infection induces selective dampening in humoral immunity with the suppression of Tfh differentiation.T richinella species are parasitic nematodes for many mammalian hosts, including humans (1). After the ingestion of muscle tissues contaminated with the muscle larval form of Trichinella, the larvae develop into adult worms by molting in the small intestine of the host. Female adult worms invade the intestinal tissue to release newborn larvae. Newborn larvae systemically migrate in the host body to striated muscle cells, resulting in survival for many years (2). Trichinella are thought to establish long-term parasitism by escaping elimination through alterations in host immune responses (3, 4). There are several species of Trichinella; some develop in muscle cells that become encapsulated (e.g., Trichinella spiralis and T. britovi) and others in cells that do not encapsulate (e.g., Trichinella pseudospiralis). Although both types of Trichinella survive in the host muscle tissues for long periods of time, the strategies for their survival may be different. Indeed, the infected host mounts an immune response to the infection with both types of Trichinella, but each immune response is different, possibly due to the different forms of immunomodulation shown by each Trichine...

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