Chemokines in inflammatory states

Chemokines probably mediate inflammation in asthma by acting on endothelial cells, alveolar cells, neutrophils, eosinophils, basophils, mast cells, monocytes, and lymphocytes, which are inhibited by corticosteroids. In 1995, we found that MCP-1 provokes mast cell aggregation and [H-3]5HT-release in cultured mast cells. In another study, MCP-1 and RANTES revealed to have a potent chemoattractive effect on basophilic cells originating from the rat skin. In this inflammatory model, RANTES also attracted eosinophils and macrophages along with basophilic cells. The effect of RANTES on inducing HDC mRNA was dose dependent. MCP-1 and RANTES provoked histamine release in intradermal mast cells and prostaglandin D2 generation. These effects clearly show that RANTES and MCP-1 are mediators of acute inflammatory responses. In chronic inflammatory reactions, MCP-1 is also present as we show in a study recently publoished by our group. In this paper, we found that MCP-1, strongly mediates the recruitment of mononuclear cells in the granuloma formed by KMnO4. In addition, MCP-1 mediated a parasitic infection caused by Trichinella spiralis in mice. Our data strongly demonstrate that chemokines, such as RANTES and MCP-1, mediate acute inflammatory response.