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TUMOR necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of rheumatoid arthritis. The present study was to evaluate the effects of lipopolysaccharide (LPS), phytomitogens and cytodifferentiation agents on cytotoxicity of TNF-alpha secreted by adherent human mononuclear cells (AMC). TNF-alpha cytotoxicity in LPS-treated, phytomitogen-treated, and cytodifferentiation agent-treated AMC supernatants were analyzed by the L929 bioassay system. Our results showed that LPS could induce homogeneous TNF-alpha production by AMC whereas, in addition to TNF-alpha, phytomitogens could also induce other TNF-like factors. Neither methotrexate, retinoic acid nor sodium butyrate can inhibit TNF-alpha cytotoxicity, while hexamethylene bisacetamide could not only inhibit TNF-alpha cytotoxicity but also TNF-alpha inducing ability of LPS to AMC.

mediators of inflammation

Establishment of a consistent L929 bioassay system for TNF-<i>α</i> quantitation to evaluate the effect of lipopolysaccharide, phytomitogens and cytodifferentiation agents on cytotoxicity of TNF-<i>α</i> secreted by adherent human mononuclear cells

Establishment of a consistent L929 bioassay system for TNF-α quantitation to evaluate the effect of lipopolysaccharide, phytomitogens and cytodifferentiation agents on cytotoxicity of TNF-α secreted by adherent human mononuclear cells