Retinoic acid differentially regulates interleukin-1β and interleukin-1 receptor antagonist production by human alveolar macrophages
1998; Elsevier BV; Volume: 22; Issue: 11 Linguagem: Inglês
10.1016/s0145-2126(98)00119-2
ISSN1873-5835
AutoresShu Hashimoto, Shinichi Hayashi, Sachiko Yoshida, Kousei Kujime, Shuichiro Maruoka, Ken Matsumoto, Yasuhiro Gon, Toshiya Koura, Takashi Horie,
Tópico(s)Neutrophil, Myeloperoxidase and Oxidative Mechanisms
ResumoMechanism in the pathogenesis of acute respiratory distress syndrome which is the clinical feature of pulmonary involvement in retinoic acid (RA) syndrome has been investigated. Pulmonary infiltration of matured 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-1β and IL-1ra production by human alveolar macrophages in order to clarify the mechanism in pulmonary infiltration of neutrophils, since IL-1 has been shown to initiate neutrophil recruitment into the lung through up-regulated expression of adhesion molecules on vascular endothelium. RA enhanced IL-1β and inhibited IL-1ra production by 4β phorbol 12β-myristate-13α acetate (PMA)- and lipopolysaccharide (LPS)-stimulated human alveolar macrophages. These results show that RA differentially regulates IL-1β and IL-1ra production by alveolar macrophages and indicate that an imbalanced production between IL-1β and IL-1ra may contribute to initiating neutrophil recruitment into the lung through up-regulated expression of adhesion molecules.
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