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Interleukin‐4 inhibits lipopolysaccharide‐induced expression of prostaglandin H synthase‐2 in human alveolar macrophages
Author(s) -
Yano Tatsutoshi,
Hopkins Harvey A.,
Hemplel Stephen L.,
Monick Martha,
Hunninghake Gary W.
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041650110
Subject(s) - lipopolysaccharide , chemistry , prostaglandin e2 , alveolar macrophage , atp synthase , microbiology and biotechnology , immunology , macrophage , biology , biochemistry , endocrinology , enzyme , in vitro
Several studies have shown that interleukin‐4 (IL‐4) down‐regulates synthesis of prostaglandin E 2 (PGE 2 ). We evaluated the mechanisms for this suppression in human alveolar macrophages (HAMs). Normal HAMs were obtained from healthy nonsmoking volunteers. The cells either remained unstimulated, or were exposed to 10 μg/ml of lipopolysaccharide (LPS) and/or various amounts of IL‐4. LPS alone induced the synthesis of large amounts of PGE 2 and prostaglandin H synthase‐2 (PGHS‐2) protein. This effect of LPS was suppressed by increasing amounts of IL‐4. Expression of LPS‐induced PGHS‐2 mRNA was also inhibited by IL‐4. In addition, IL‐4 inhibited expression of CD14, which is a receptor for LPS bound to the LPS‐binding protein (LBP). We conclude that IL‐4 down‐regulates LPS‐induced release of PGE 2 , by reducing expression of the enzyme, PGHS‐2. One potential mechanism for this effect of IL‐4 is a reduced expression of CD14, which is the LPS‐LBP receptor. © 1995 Wiley‐Liss Inc.