The IL-4/13-induced production of M2 chemokines by human lung macrophages is enhanced by adenosine and PGE2

CCL22 Macrophage inflammatory protein
DOI: 10.1016/j.intimp.2024.111557 Publication Date: 2024-01-23T22:24:10Z
ABSTRACT
Lung macrophages (LMs) are critically involved in respiratory diseases. The primary objective of the present study was to determine whether or not an adenosine analog (NECA) and prostaglandin E2 (PGE2) affected interleukin (IL)-4- IL-13-induced release M2a chemokines (CCL13, CCL17, CCL18, CCL22) by human LMs. Primary isolated from resected lungs were incubated with NECA, PGE2, roflumilast, vehicle stimulated IL-4 IL-13 for 24 h. levels PGE2 culture supernatants measured using ELISAs enzyme immunoassays. Exposure (10 ng/mL) (50 associated greater chemokine production but production. NECA (10-6 M) induced a lesser extent significantly enhanced IL-4/IL-13-induced these chemokines. At either clinically relevant concentration (10-9 at (10-7 that fully inhibited phosphodiesterase 4 (PDE4) activity, roflumilast did increase modulate their production, regardless presence absence PGE2. inhibition PDE4 alter These results contrast totally previously reported inhibitory effects inhibitors on lipopolysaccharide-induced tumor necrosis factor alpha M1
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