| First Author | Rovai LE | Year | 1998 |
| Journal | J Leukoc Biol | Volume | 64 |
| Issue | 4 | Pages | 494-502 |
| PubMed ID | 9766630 | Mgi Jnum | J:50201 |
| Mgi Id | MGI:1290022 | Doi | 10.1002/jlb.64.4.494 |
| Citation | Rovai LE, et al. (1998) The murine neutrophil-chemoattractant chemokines LIX, KC, and MIP-2 have distinct induction kinetics, tissue distributions, and tissue-specific sensitivities to glucocorticoid regulation in endotoxemia. J Leukoc Biol 64(4):494-502 |
| abstractText | Lipopolysaccharide-induced CXC chemokine (LIX) is a novel murine neutrophil-chemo-attractant CXC chemokine cloned as a glucocorticoid-attenuated response gene. We investigated LIX message expression in an acute endotoxemia model. LIX message peaks later than KC or macrophage inflammatory protein-2 (MIP-2) and remains elevated longer in almost all tissues. Induced LIX message expression in heart is 5- to 6-fold greater than in lung and spleen, and 20-fold greater than in liver. In contrast, KC expression is equal in heart, lung, and liver, whereas MIP-2 expression is strongest in the lung. Glucocorticoid regulation of these genes also differs. Endotoxemia-induced LIX message expression in the lung is markedly enhanced in adrenalectomized mice and strongly attenuated by dexamethasone, whereas lung KC and MIP-2 expression are unaffected by glucocorticoids. It is surprising to note that endotoxemia-induced brain expression of LIX (but not KC or MIP-2) is increased by dexamethasone. These observations suggest that LIX may have biological roles distinct from KC and MIP-2. |
