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Viscum album agglutinin‐I induces apoptosis and degradation of cytoskeletal proteins via caspases in human leukaemia eosinophil AML14.3D10 cells: differences with purified human eosinophils
Author(s) -
Lavastre Valérie,
Chiasson Sonia,
Cavalli Hélène,
Girard Denis
Publication year - 2005
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2005.05633.x
Subject(s) - apoptosis , biology , caspase , gelsolin , microbiology and biotechnology , eosinophil , inhibitor of apoptosis domain , programmed cell death , immunology , biochemistry , actin , asthma
Summary Although there are several agents that induce neutrophil apoptosis, few are known as inducers of eosinophil apoptosis. As eosinophils are potent effector cells contributing to allergic inflammation and asthma, we investigated whether the pro‐apoptotic agent Viscum album agglutinin‐I (VAA‐I) could induce eosinophil apoptosis. VAA‐I was found to induce apoptosis in eosinophilic AML14.3D10 (3D10) cells and that these cells expressed caspases‐1, ‐2, ‐3, ‐4, ‐7, ‐8, ‐9 and ‐10. VAA‐I‐induced gelsolin degradation was reversed by the pan‐caspase inhibitor N ‐benzyloxycarbonyl‐V‐A‐D‐O‐methylfluoromethyl ketone (z‐VAD). Also, paxillin, vimentin and lamin B 1 were cleaved by caspases in VAA‐I‐induced 3D10 cells. VAA‐I activated caspase‐3 and ‐8 in 3D10 cells but, unlike z‐VAD, treatment with a caspase‐8 inhibitor slightly reversed apoptosis. Treatment of purified human eosinophils with VAA‐I was found to induce apoptosis, degradation of gelsolin and lamin B 1 , but unlike 3D10 cells, cleavage of lamin B 1 and cell apoptosis was not reversed by z‐VAD. We conclude that VAA‐I is a potent inducer of eosinophil apoptosis and that proteases other than those inhibited by z‐VAD in 3D10 cells are involved in VAA‐I‐induced peripheral blood eosinophil apoptosis and lamin B 1 cleavage. Thus, VAA‐I represents a potential candidate for the reduction of the number of eosinophils in diseases where they play important roles.