Eosinophils, originating from bone-marrow stem cells, appear in large numbers at inflammation sites and in response to certain parasitic infections. These leukocytes, when mature, reside mostly in tissues, but about 1% of the eosinophil population circulates in the blood. Activated eosinophils degranulate to release four highly basic proteins into the surrounding tissue. The granular proteins, which can kill parasites and some mammalian cells, might cause the tissue damage associated with asthma and other inflammatory diseases. Eosinophil activation accompanies a wide range of inflammatory conditions, including bronchial asthma, atopic dermatitis, rhinitis, allergic eye inflammation, allergic middle ear effusion, parasitic and bacterial infections, autoimmune diseases, and chronic fatigue syndrome.
Among the four basic granule proteins, eosinophil cationic protein (ECP) has proven a useful monitor for many active 11 inflammatory diseases. ECP concentrations in plasma and certain other body fluids increase during inflammatory reactions marked by activated eosinophils. Produced by eosinophils exclusively, ECP is toxic to neurons, some epithelial cell lines, and isolated myocardial cells. The positively charged protein binds to heparin and inhibits blood coagulation.
Several studies report high individual and group correlations between ECP levels and clinical asthma symptoms, such as increases in peak expiratory flow (PEF), prn ("as needed") inhaled β2-agonist, airway responsiveness, and spirometry. Atopic serum samples have higher ECP levels than nonatopic control samples, even when the circulating eosinophil count remains within the normal range. In seasonal asthmatic patients, ECP measurements reflect changes in disease activity throughout the year. Roquet, et al. reported significant correlations between ECP levels and bronchial hyperreactivity in mildly asthmatic patients. Tomassini, et al. showed that serum ECP concentrations exceed normal, control levels in both IgE- mediated and non-IgE-mediated atopic conditions. Serum ECP measurements avoid inconsistencies inherent in subjective asthma assessments.
Serum ECP concentrations can indicate the severity of certain skin disorders. ECP's neuronal toxicity might contribute to itching disorders; patients with certain skin disorders, such as papular erythematous eruptions and prurigo nodularis, displayed increased serum ECP levels, which normalized when the conditions healed. Several groups found that serum ECP concentrations reflect atopic dermatitis (AD) activity. The commonly used clinical scoring system for atopic dermatitis records lichenification, loss of sleep, erythema, papules, pruritus, and excoriations. Czech, et al. showed that ECP correlates with each of these symptoms and most highly correlates with the total clinical score. Although altered immunological parameters accompany atopic dermatitis, measured serum IgE concentrations did not correlate with some of the clinical symptoms. The objective nature of serum ECP measurements presents an advantage over the subjective clinical measures, which are prone to inconsistencies arising from the broad range in individual investigator and patient assessments.