Possible role of LECT2 as an intrinsic regulatory factor in SEA-induced toxicity in d-galactosamine-sensitized mice
Copyright © 2010 Elsevier Inc. All rights reserved.
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 137(2010), 3 vom: 01. Dez., Seite 311-21 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , , , , , , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2010
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Enterotoxins Intercellular Signaling Peptides and Proteins Interleukin-6 Lect2 protein, mouse Tumor Necrosis Factor-alpha enterotoxin A, Staphylococcal 37337-57-8 Galactosamine |
| Zusammenfassung: | Copyright © 2010 Elsevier Inc. All rights reserved. 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 |
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| Beschreibung: | Date Completed 26.11.2010 Date Revised 25.11.2016 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2010.08.002 |