RETINOIC ACID DIFFERENTIALLY REGULATES INTERLEUKIN-1-BETA AND INTERLEUKIN-1 RECEPTOR ANTAGONIST PRODUCTION BY HUMAN ALVEOLAR MACROPHAGES

Mechanism in the pathogenesis of acute respiratory distress syndrome w hich is the clinical feature of pulmonary involvement in retinoic acid (RA) syndrome has been investigated. Pulmonary infiltration of mature d neutrophils and leukemic cells is thought to be associated with the pathogenesis of pulmonary involvement in RA syndrome; however. Little is known about the mechanism in pulmonary infiltration of these cells. In the present study, we examined the effect of RA on IL-1 beta and I L-1ra production by human alveolar macrophages in order to clarify the mechanism in pulmonary infiltration of neutrophils, since IL-1 has be en shown to initiate neutrophil recruitment into the lung through up-r egulated expression of adhesion molecules on vascular endothelium. RA enhanced IL-1 beta and inhibited IL-1ra production by 4 beta phorbol 1 2 beta-myristate-13 alpha acetate (PMA)- and lipopolysaccharide (LPS)- stimulated human alveolar macrophages. These results show that RA diff erentially regulates IL-1 beta and IL-1ra production by alveolar macro phages and indicate that an imbalanced production between IL-1 beta an d IL-1ra may contribute to initiating neutrophil recruitment into the lung through up-regulated expression of adhesion molecules. (C) 1998 E lsevier Science Ltd. All rights reserved.