Mast cells are found in the skin and in all mucosal tissues at homeostasis, and numbers are elevated in asthmatics lungs [49] . Mast cell and eosinophil numbers in mucosa are correlated to bronchial hyperactivity (BHR) [89] and mast cell products and eosinophil MBP but not ECP induces BHR [90] . Several lines of evidence suggest that there is a cross talk between eosinophils and mast cells [91] which to some extent are related to ECP release. Mast cells produce and secrete IL-5, PAF and LTB 4 known to augment ECP release from eosinophils. Rat peritoneal mast cells on the other hand incubated with moderate levels of ECP (0. 9 μM/17 μg/mL) for 45 min released 50 percent of their histamine. Histamine is not released from peripheral basophils by ECP treatment (as by MBP) [92] . However, the release of histamine may be location specific as no release was observed from human skin mast cells treated with up to 200 μg/ mL ECP [93] . Histamine and of some tryptase was though released from human heart mast cells, purified from traffic victims or from individuals undergoing heart transplantation, when stimulated with moderate levels of ECP (2.5 μM; 4.7 μg/mL). Between 10 and 80 percent of preformed mediators were released from these cells and MBP had a similar effect whereas EPX/ EDN did not induce any release [94] . This ECP induced histamine release occurred within 60 sec of stimulation and was found to be Ca 2+ -, temperature-and energy dependent, and ECP was not toxic to the cells. Another mast cell product, prostaglandin D 2 (PGD 2 ) was synthesised de novo by the same amount of ECP added. PGD 2 is a chemoattractant for eosinophils and TH2 lymphocytes, through binding the CRTH2 receptor [95] . Therefore these findings suggest that in some tissue the interactions between mast cells and eosinophils can be attributed to the positive feedback of ECP release.