PubMed · 7100717
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A Luyckx, A Scheen, H van Cauwenberge. 1982-05-01. [Current therapeutic agents].. https://pubmed.ncbi.nlm.nih.gov/7100717/
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Leumedins are small molecules that inhibit neutrophil movement into inflamed tissues. These compounds have been shown to inhibit the adherence of neutrophils in static adhesion assays mediated by beta2-integrins. We now report that leumedins, like activating agents, induce the loss of L-selectin from the neutrophil surface. The loss of L-selectin is unrelated to the inhibition of static adhesion, since neutrophils that have been pretreated with leumedins to cause shedding of L-selectin, followed by removal of drug, adhere normally in a static adhesion assay, and this adhesion is inhibited upon readdition of leumedin. In an assay of adhesion to endothelial cells under conditions of physiologic wall shear stress, leumedins prevent both primary capture of neutrophils mediated by L-selectin and firm adherence mediated by beta2-integrins.
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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.