These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Neutrophil-activating protein ENA-78 and IL-8 exhibit different patterns of expression in lipopolysaccharide- and cytokine-stimulated human monocytes. Author: Schnyder-Candrian S, Walz A. Journal: J Immunol; 1997 Apr 15; 158(8):3888-94. PubMed ID: 9103458. Abstract: The production of epithelial neutrophil-activating protein-78 (ENA-78) by normal human monocytes was studied in comparison with IL-8 upon stimulation with various stimuli. LPS at 100 ng/ml was a strong inducer of ENA-78, yielding a delayed up-regulation of steady state mRNA peaking at 24 h and causing a long-lasting ENA-78 protein secretion starting 20 h after induction. As shown by specific ELISA and immunoprecipitation, ENA-78 secretion by monocytes was not down-regulated for up to 72 h. Thus, ENA-78 production becomes effective when IL-8 synthesis is shut off, since IL-8 mRNA peaks at 4 to 12 h and approaches background levels at about 16 h. Induction of steady state ENA-78 mRNA by proinflammatory cytokines IL-1beta (10 ng/ml) and TNF-alpha (100 ng/ml) was weaker than that by LPS and yielded a biphasic kinetic with a first maximum at 8 to 12 h and a second at 20 to 28 h. Steady state IL-8 mRNA induced by LPS, IL-1beta, or TNF-alpha was superinduced or unchanged in the presence of cycloheximide (10 microg/ml). In contrast, ENA-78 mRNA was completely abrogated, suggesting the involvement of a newly synthesized protein intermediate necessary for ENA-78 up-regulation. Dexamethasone treatment reduced ENA-78 mRNA and protein levels by 60% of the LPS control level. This inhibition was identical when dexamethasone was added 8 h after LPS induction. These results demonstrate significant differences in the production of monocyte-derived IL-8 and ENA-78 and thus may suggest different roles for the two chemokines in acute or chronic inflammation.[Abstract] [Full Text] [Related] [New Search]