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Structural Alterations in Fibroblast Monolayers Caused by Mast Cell Degranulation
Author(s) -
Ginsburg Haim,
Amira Milly,
Padawer Jacques,
Davidson Sima
Publication year - 1989
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.45.6.491
Subject(s) - degranulation , biology , chymase , mast cell , histamine , fibroblast , extracellular , microbiology and biotechnology , cytoplasm , cell culture , immunology , endocrinology , biochemistry , receptor , genetics
Populations of mature, long‐lived, nondividing mast cells develop on embryonic fibroblast monolayers after 1 mo growth of lymph node cells taken from mice immunized with horse serum. Total mast cell degranulation with 80‐90% histamine release has been obtained by monoclonal anti‐2,4‐dinitrophenol (anti‐DNP) IgE and the antigen. This degranulation process was studied by time‐lapse cinematography and scanning electron microscopy. Excitation of the mast cells began as early as 10 s after addition of the antigen and lasted for about 15 s. Consequently, the fibroblast cytoplasm was displaced by short 5‐10 s movements. Before degranulation, due to an extracellular film that coated the cells and the extracellular fibers, the monolayer appeared as a continuous, uninterrupted layer. After degranulation and fibroblast cytoplasm displacement, the fibrous network was exposed. Several inhibitors and antagonists of mast cell mediators were introduced to the cultures prior to addition of the antigen. So far, only with soybean trypsin inhibitor was the cytoplasm dislocation inhibited. Histamine H 1 and H 2 and serotonin receptor antagonists, as well as indomethacin, Cortisol, aprotinin, and phenylmethylsulfonyl fluoride, did not inhibit. These results suggest that chymase, which constitutes the greater part of the mast cell granule protein, is the causative agent.