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Lipopolysaccharide and a phorbol ester stimulate secretion of tumor necrosis factor‐α from alveolar macrophages through action on overlapping subsets of cells
Author(s) -
Taylor Michael J.,
Hehnke Karen,
Clark Cheryl L.
Publication year - 1993
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.54.5.384
Subject(s) - lipopolysaccharide , tumor necrosis factor alpha , secretion , incubation , pulmonary alveolus , phorbol , biology , endocrinology , medicine , tumor necrosis factor α , microbiology and biotechnology , immunology , macrophage , in vitro , biochemistry , protein kinase c , signal transduction
A cell‐by‐cell analysis of the secretory ability of stimulated, individual alveolar macrophages (AMs) was performed through use of a tumor necrosis factor a (TNF‐α) reverse hemolytic plaque assay. Two functional end points were measured: the percentage of AMs that were TNF‐α secretors and the cumulative amount of TNF‐α secreted by AMs (average plaque area, μm 2 ). Lipopolysaccharide (LPS; 100 μg/ml) increased cumulative TNF‐α release at both 7 and 20 h of incubation. On the other hand, a phorbol ester (phorbol myristate acetate, PMA) stimulated TNF‐α release at 20 h of incubation but not at 7 h. Under nonstimulated culture conditions, 5‐10% of all AMs released detectable TNF‐α. PMA (but not LPS) induced a significant increase in the fraction of AMs capable of releasing TNF‐α (15.1 ± 1.1% vs. 9.0 ± 1.6%, PMA vs. control, P < .05). Differences in the time course of secreted TNF‐α, together with the recruiting effect of PMA, suggest that LPS and PMA target TNF‐α‐ secretory subpopulations of AMs that differ in number and secretory characteristics.