Mice lacking α1,3-fucosyltransferase 9 exhibit modulation ofin vivoimmune responses against pathogens


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Abstract

Carbohydrate structures, including Lewis X (Lex), which is not synthesized in mutant mice that lack α1,3-fucosyltransferase 9 (Fut9−/−), are involved in cell–cell recognition and inflammation. However, immunological alteration in Fut9−/− mice has not been studied. Thus, the inflammatory response of Fut9−/− mice was examined using the highly neurovirulent mouse hepatitis virus (MHV) JHMV srr7 strain. Pathological study revealed that inflammation induced in the brains of Fut9−/− mice after infection was more extensive compared with that of wild-type mice, although viral titers obtained from the brains of mutant mice were lower than those of wild-type mice. Furthermore, the reduction in cell numbers in the spleens of wild-type mice after infection was not observed in the infected Fut9−/− mice. Although there were no clear differences in the levels of cytokines examined in the brains between Fut9−/− and wild-type mice except for interferon-β expression, some of those in the spleens, including interferon-γ, interleukin-6, and monocyte chemoattractant protein 1, showed higher levels in Fut9−/− than in wild-type mice. Furthermore, Fut9−/− mice were refractory to thein vivoinoculation of endotoxin (LPS) compared with wild-type mice. These results indicate that Lex structures are involved in host responses against viral or bacterial challenges.

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