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

Lipopolysaccharide‐induced CXC chemokine (LIX) is a novel murine neutrophil‐chemoattractant 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. J. Leukoc. Biol. 64: 494–502; 1998.