Friday, 21 October 2011

ECP/EDN ELISA: Eosinophil and bronchial asthma


The pathology of bronchial asthma suggests bronchial inflammation is mainly caused by leukocytes and eosinophils.
Eosinophils and leukocytes are recognized as permeating tunica mucosa bronchiorum in patients with chronic bronchial asthma in both atopic and non-atopic conditions. When stimulated, the respiratory epithelial cells induce production and release various cytokines. Cytokines such as granulocyte-macrophage colony stimulating factors (GM-CSF) retain biological activities for eosinophils; their activities can include maturity, differentiation, migration and life prolongation. Activated eosinophils secrete granular proteins that injure and exfoliate the respiratory epithelium. They also release active oxygen with the ability of injuring cells, which can constrict bronchial smooth muscle and platelet-activating factors attractive for eosinophils and neutrophils. As a result, these substances cause bronchoconstriction, hyper transmission of blood vessels and hypersecretion of mucus.

Eosinophil Cationic Protein (ECP), Eosinophil Derived Neurotoxin (EDN) and Major Basic Protein (MBP) are known to be major protein-mediators derived from activated eosinophils. Activated eosinophils play an important role in inflammatory processes especially in allergic diseases. The levels of eosinophil activation can serve as complementary data for monitoring asthma inflammation. As ECP/EDN proteins are secreted from activated eosinophils they can become markers of eosinophil activation and degranulation which can cause inflammatory disease of the airway.


  • No cross reactivity with EDN
  • For use with human serum samples
  • No cross reactivity with ECP
  • For use with human serum samples

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