Author/Authors :
Dang، نويسنده , , Minh Hung and Kato، نويسنده , , Hidehito and Ueshiba، نويسنده , , Hidehiro and Omori-Miyake، نويسنده , , Miyuki and Yamagoe، نويسنده , , Satoshi and Ando، نويسنده , , Kazuyoshi and Imanishi، نويسنده , , Kenʹichi and Arimura، نويسنده , , Yutaka and Haruta، نويسنده , , Ikuko and Kotani، نويسنده , , Tohru and Ozaki، نويسنده , , Makoto and Suzuki، نويسنده , , Kazuo and Uchiyama، نويسنده , , Tak، نويسنده ,
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/6 J (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.
Keywords :
LECT2 , Staphylococcal enterotoxin A , multiple organ failure , Toxic shock syndrome , inflammation , Liver Failure , DIC , cytokines
