The role of eosinophils in asthma has been under scrutiny since clinical trials showing that anti-IL-5 therapy did not improve the disease symptoms for allergic asthmatics albeit eosinophil numbers were reduced [150] . However, two recent clinical trials have shown that anti-IL-5 antibodies actually could relieve symptoms in eosinophil rich, late onset asthma, suggesting that eosinophils can have a pathogenic role in this disease. In these trials inflammatory exacerbations were reduced when anti-IL-5 antibodies were administrated [151, 152] . Earlier studies using diagnostic ECP measurements seem to agree with these findings as ECP levels correlate with severity of asthma: FEV (sputum ECP) [70] , need for GC treatment (sputum ECP) [153] and blood eosinophilia (sECP) [71] . Results from in vitro studies presented in this review may well suggest several roles for ECP in this type of allergic asthma. The protein might act as an inflammatory amplifier by augmentation of release of, for eosinophils chemotactic, PGD 2 from mast cells in asthmatic patients. Moreover, protein released in the interstitium might influence fibrosis development ( Figure 3B , 4B and 5). One might speculate that blocking antibodies to ECP could be a symptom relieving addition to the already established GC and anti-IL5 therapies used in eosinophil rich asthma and other eosinophilic diseases [113, 151, 152] . Table 2 shows that the level of protein needed to influence proliferation of lymphocytes and their antibody production is 1000 times lower than the destructive levels described above, i.e. in the ng/mL range. In murine system eosinophils have been ascribed a novel role in inflammation; the cells enter and contribute to the well orchestrated process of inflammation resolution of by release of the pro-resolving lipid protectin D1 [154] (for a review see [155] ). Whether ECP is released during this resolution process for the dual role of sequestering subpopulations of inflammatory lymphocytes [86] and promoting tissue repair by TGF beta augmentation [81] is an intriguing speculation. Eosinophils are also present at homeostasis at low numbers in lymphocyte rich organs at various locations but degranulated only in the GI tract [50] . A single eosinophil contains 13 pg ECP. Do eosinophils have a role in maintaining homeostasis and do low levels of ECP also have a role here? EDN, the sister protein has been found to play an active role during inflammation development influencing the maturation of DC's [37] . If EDN is proinflammatory, perhaps the two proteins divergence could be because ECP might have acquired a novel role as yet unknown role.