Interactions of Cytokines and Lipid Mediators in Acute and Chronic Inflammation

Priming Cytokines Colony-stimulating factors Lipid mediators Atopy Correspondence to: Prof. Dr. med. W. König, Ruhr-Universität Bochum Medizinische Fakultät, Abt. für Med. Mikrobiologie und Immunologie, Universitätsstrasse 150, D–44780 Bochum (Germany) We analysed the effects of the growth factors granulo-cyte/macrophage-colony-stimulating factor (GM-CSF) and granulocyte-colony-stimulating factor (G-CSF), as well as the cytokines interleukin (IL)-3 and IL-8 on the generation of leukotriene (LT)B4 and IL-8 from human peripheral blood cells after subsequent stimulation with N-formyl-methionyl-leucylphenylalanine (fMLP). The amounts of LTB4 generated from neutrophils (PMNs) and from the lymphocyte-monocyte-basophil fraction (LMB) from patients with atopic dermatitis (AD), with type 1 allergic diseases or psoriasis (PD) were compared with those of normal donors. Our results demonstrate that the cells from patients with AD [ 1,2] or type 1 allergy generated significantly higher quantities of inflammatory lipid mediators as compared to cells from normal donors or from psoriatic patients (tables 1-3). Unlike the Ca ionophore A23187, stimulation of PMNs or LMBs with fMLP or fluoride led to a diminished formation of LTB4 in the presence of cetirizine 2HC1. Furthermore transcellular metabolism of LTA4 by platelets into LTC4, D4, and E4 was markedly suppressed by cetirizine 2HC1. Costimulation of PMN/platelet or LMB/platelet suspensions from normal and atopic donors also led to a suppression for leukotriene and IL-8 release in the presence of cetirizine. Since cetirizine inhibited receptormediated cell Table 1. Formation of LTB4 (ng/l×107 PMNs) after priming with IL-3, IL-8, and GM-CSF without or with LTA4