title: Mice lacking α1,3-fucosyltransferase 9 exhibit modulation of in vivo immune responses against pathogens.
abstract: Carbohydrate structures, including Lewis X (Le(x)), 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 the in vivo inoculation of endotoxin (LPS) compared with wild-type mice. These results indicate that Le(x) structures are involved in host responses against viral or bacterial challenges.
authors.affiliation: Department of Bioinformatics, Faculty of Engineering, Soka University, Hachioji, Tokyo, Japan.
authors.forename: Hiromi
authors.initials: H
authors.lastname: Kashiwazaki
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Kakizaki
authors.forename: Yuzuru
authors.initials: Y
authors.lastname: Ikehara
authors.forename: Akira
authors.initials: A
authors.lastname: Togayachi
authors.forename: Hisashi
authors.initials: H
authors.lastname: Narimatsu
authors.forename: Rihito
authors.initials: R
authors.lastname: Watanabe
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology / Q000821:virology; D002452:Cell Count; D018352:Coronavirus Infections / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005647:Fucosyltransferases / Q000172:deficiency* / Q000235:genetics / Q000502:physiology; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology* / Q000502:physiology; D008070:Lipopolysaccharides / Q000276:immunology*; D051379:Mice; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D006517:Murine hepatitis virus / Q000276:immunology* / Q000302:isolation & purification; D013154:Spleen / Q000473:pathology / Q000821:virology
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D005647:Fucosyltransferases; C518194:fucosyltransferase 9, mouse
keywords: Fut9; Lewis X; MHV; cytokine; neuropathogenic virus