title: Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice.
abstract: To elucidate whether leukocyte cell-derived chemotaxin 2 (LECT2) controls the progression of staphylococcal enterotoxin A (SEA)-induced toxicity, we examined the role of LECT2 in a mouse model. Almost all the C57BL/6J (B6) mice survived for 72 h after the injection of 0.1 μg of SEA and 20 mg of d-galactosamine (d-GalN). However, the same treatment protocol in LECT2(-/-) mice produced a high lethality (~90%), severe hepatic apoptosis, and massive hepatic and pulmonary hemorrhage, similar to the situation observed in B6 mice treated with 1.0 μg SEA/d-GalN. The plasma LECT2 levels in B6 mice treated with 1.0 μg SEA/d-GalN were inversely correlated with the plasma cytokine levels and were associated with prognosis. LECT2 administration increased the survival of B6 mice and down-regulated TNF-α and IL-6. These results suggest the involvement of LECT2 in the regulation of fatal SEA-induced toxicity in d-GalN-sensitized mice.
authors.affiliation: Department of Microbiology and Immunology, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
authors.forename: Minh Hung
authors.initials: MH
authors.lastname: Dang
authors.forename: Hidehito
authors.initials: H
authors.lastname: Kato
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Ueshiba
authors.forename: Miyuki
authors.initials: M
authors.lastname: Omori-Miyake
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamagoe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Ando
authors.forename: Ken'ichi
authors.initials: K
authors.lastname: Imanishi
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Arimura
authors.forename: Ikuko
authors.initials: I
authors.lastname: Haruta
authors.forename: Tohru
authors.initials: T
authors.lastname: Kotani
authors.forename: Makoto
authors.initials: M
authors.lastname: Ozaki
authors.forename: Kazuo
authors.initials: K
authors.lastname: Suzuki
authors.forename: Takehiko
authors.initials: T
authors.lastname: Uchiyama
authors.forename: Junji
authors.initials: J
authors.lastname: Yagi
mesh_terms: D000818:Animals; D017209:Apoptosis; D056486:Chemical and Drug Induced Liver Injury / Q000276:immunology / Q000473:pathology*; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000187:drug effects / Q000276:immunology; D004768:Enterotoxins / Q000276:immunology / Q000633:toxicity; D005260:Female; D005434:Flow Cytometry; D005688:Galactosamine / Q000276:immunology*; D006470:Hemorrhage / Q000139:chemically induced; D020287:In Situ Nick-End Labeling; D036341:Intercellular Signaling Peptides and Proteins / Q000008:administration & dosage / Q000276:immunology* / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D012772:Shock, Septic / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004768:Enterotoxins; D036341:Intercellular Signaling Peptides and Proteins; D015850:Interleukin-6; C491213:Lect2 protein, mouse; D014409:Tumor Necrosis Factor-alpha; C026066:enterotoxin A, Staphylococcal; D005688:Galactosamine