7 research outputs found

    Involvement of resistin-like molecule ╬▓ in the development of methionine-choline deficient diet-induced non-alcoholic steatohepatitis in mice

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    Resistin-like molecule ╬▓ (RELM╬▓) reportedly has multiple functions including local immune responses in the gut. In this study, we investigated the possible contribution of RELM╬▓ to non-alcoholic steatohepatitis (NASH) development. First, RELM╬▓ knock-out (KO) mice were shown to be resistant to methionine-choline deficient (MCD) diet-induced NASH development. Since it was newly revealed that Kupffer cells in the liver express RELM╬▓ and that RELM╬▓ expression levels in the colon and the numbers of RELM╬▓-positive Kupffer cells were both increased in this model, we carried out further experiments using radiation chimeras between wild-type and RELM╬▓-KO mice to distinguish between the contributions of RELM╬▓ in these two organs. These experiments revealed the requirement of RELM╬▓ in both organs for full manifestation of NASH, while deletion of each one alone attenuated the development of NASH with reduced serum lipopolysaccharide (LPS) levels. The higher proportion of lactic acid bacteria in the gut microbiota of RELM╬▓-KO than in that of wild-type mice may be one of the mechanisms underlying the lower serum LPS level the former. These data suggest the contribution of increases in RELM╬▓ in the gut and Kupffer cells to NASH development, raising the possibility of RELM╬▓ being a novel therapeutic target for NASH

    Animal models of Multiple Sclerosis

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    Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) which involves a complex interaction between immune system and neural cells. Animal modeling has been critical for addressing MS pathogenesis. The three most characterized animal models of MS are (1) the experimental autoimmune/allergic encephalomyelitis (EAE); (2) the virally-induced chronic demyelinating disease, known as TheilerÎ│s murine encephalomyelitis virus (TMEV) infection and (3) the toxin-induced demyelination. All these models, in a complementary way, have allowed to reach a good knowledge of the pathogenesis of MS. Specifically, EAE is the model which better reflects the autoimmune pathogenesis of MS and is extremely useful to study potential experimental treatments. Furthermore, both TMEV and toxin-induced demyelination models are suitable for characterizing the role of the axonal injury/repair and the remyelination process in MS. In conclusion, animal models, despite their limitations, remain the most useful instrument for implementing the study of MS
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