| First Author | Dang MH | Year | 2010 |
| Journal | Clin Immunol | Volume | 137 |
| Issue | 3 | Pages | 311-21 |
| PubMed ID | 20805039 | Mgi Jnum | J:167098 |
| Mgi Id | MGI:4867151 | Doi | 10.1016/j.clim.2010.08.002 |
| Citation | Dang MH, et al. (2010) Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice. Clin Immunol 137(3):311-21 |
| abstractText | 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 mug 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 mug SEA/d-GalN. The plasma LECT2 levels in B6 mice treated with 1.0 mug 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-alpha and IL-6. These results suggest the involvement of LECT2 in the regulation of fatal SEA-induced toxicity in d-GalN-sensitized mice. |
