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Human Neutrophil Degranulation Stimulated by Aspergillus fumigatus
Author(s) -
Levitz Stuart M.,
Farrell Timothy P.
Publication year - 1990
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.47.2.170
Subject(s) - degranulation , phagocytosis , aspergillus fumigatus , lactoferrin , respiratory burst , opsonin , biology , microbiology and biotechnology , zymosan , antibody opsonization , immunology , neutrophile , stimulation , granulocyte , in vitro , biochemistry , inflammation , receptor , endocrinology
Previous studies have established that human neutrophils (PMN) are unable to kill resting conidia (RC) of Aspergillus fumigatus but can kill conidia that have been preincubated in culture medium until swollen but not yet germinated. Compared with swollen conidia (SC), RC stimulate a relatively weak PMN respiratory burst In the present study, we further examined the mechanisms of resistance of RC to neutrophil killing by comparing neutrophil degranulation and phagocytosis following stimulation by RC and SC opsonized in pooled human serum. RC, compared with SC, stimulated significantly less release of both the primary granule marker β‐glucuronidase and the secondary granule marker lactoferrin. PMN also phagocytosed significantly greater numbers of SC, although the differences in phagocytosis were not great enough to account for the differences in degranulation. Suboptimal stimulation of degranulation and phagocytosis may thus contribute to the inability of neutrophils to kill RC. Moreover, reagent lactoferrin bound avidly to both RC and SC, raising the possibility that PMN‐released lactoferrin may contribute to antifungal activity at the conidial surface by competing for iron or catalyzing the formation of oxygen radicals.