Abstract.
Chemotaxis allows polymorphonuclear neutrophils (PMN) to rapidly reach infected and inflamed sites. However, excessive influx of PMN damages host tissues. Better knowledge of the mechanisms that control PMN chemotaxis may lead to improved treatments of inflammatory diseases. Recent findings suggest that ATP and adenosine are involved in PMN chemotaxis. Therefore, these purinergic signaling processes may be suitable targets for novel therapeutic approaches to ameliorate host tissue damage.
Keywords. Neutrophils, inflammation, chemotaxis, puringeric receptors, tissue damage
Footnotes
Received 25 February 2008, received after revision 31 March 2008, accepted 02 April 2008