A synthetic, non-peptide CXCR2 antagonist blocks MIP-2-induced neutrophil migration in mice.

Non-peptide antagonists of chemokine receptors are considered an intriguing alternative for the treatment of acute and chronic diseases. Particularly the recruitment of neutrophils to inflammatory sites often causes harmful side effects and is mediated by chemokine ligands of the CXC chemokine receptor 2 (CXCR2). Hence, this receptor has been proposed as an important target for novel drugs.

Constitutive expression of CXCL2/MIP-2 is restricted to a Gr-1high, CD11b+, CD62Lhigh subset of bone marrow derived granulocytes.

CXCL2/macrophage inflammatory protein (MIP)-2 is an inducible murine chemokine involved in attraction of polymorphonuclear granulocytes to sites of infection. In comparison, its role as constitutive produced chemokine in mice is unclear. The present study aimed to specify the cellular source of constitutively produced CXCL2/MIP-2 and to examine its expression pattern in comparison to other chemokines in peripheral lymphoid tissues as well as bone marrow (BM) of normal mice.