{'fraction_non_alphanumeric': 0.03363636363636364, 'fraction_numerical': 0.005454545454545455, 'mean_word_length': 6.103225806451613, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Cyclic Adenosine Monophosphate Decreases the Secretion, but not the Cell‐Associated Levels, of Interleukin‐1β in Lipopolysaccharide‐Activated Human Monocytes

Interleukin‐1β (IL‐1β) is a cytokine produced mainly by activated monocytes though the mechanism by which it is released is still unknown. Elevation of intracellular cyclic adenosine monophosphate (cAMP) is considered an important down‐regulative signal in the production of IL‐1β in lipopolysaccharide (LPS)‐induced monocytes. In this study we show that in LPS‐activated human monocytes, elevated cAMP concentrations (induced by either prostaglandin E2, forskolin or dibutyrylcyclic AMP) affected specifically secretion of IL‐1β; the amount of secreted IL‐β was clearly reduced whereas the cell‐associated level remained unchanged. TNF‐α, a normal secretory protein, was used as a control. Cyclic AMP also inhibited TNF production by monocytes, but the decrease was of the same magnitude in the extracellular and intracellular compartments. Thus, the down‐regulative effect of cAMP on the production of these monokines is clearly different.