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Interleukin‐4 suppresses inflammatory cytokine gene transcription in porcine macrophages
Author(s) -
Zhou Yaling,
Lin Gaofeng,
Baarsch Mary Jo,
Scamurra Ronald W.,
Murtaugh Michael P.
Publication year - 1994
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.56.4.507
Subject(s) - tumor necrosis factor alpha , lipopolysaccharide , biology , cytokine , proinflammatory cytokine , interleukin , immune system , immunology , microbiology and biotechnology , interleukin 19 , inflammation , beta (programming language) , messenger rna , alveolar macrophage , macrophage , in vitro , gene , interleukin 5 , biochemistry , computer science , programming language
Inflammatory cytokines, including interleukin (IL)‐1 α , IL‐1 β , IL‐8, and tumor necrosis factor α (TNF‐ α ) are produced by macrophages in response to a variety of pathogenic stimuli. We show here that the expression of inflammatory cytokines is suppressed by IL‐4 at the transcriptional level. Interleukin‐4, when added together with bacterial lipopolysaccharide (LPS), suppressed LPS‐induced increases in mRNA levels of IL‐1 α , IL‐1 β , IL‐8, and TNF‐ α in alveolar macrophages. The level of suppression was dependent on dose and time of exposure and reached a maximum of 75–80% of uninduced values for IL‐1 α , IL‐8, and TNF. Interleukin‐1 β expression was completely inhibited by IL‐4. The amount of secreted protein, as determined by TNF‐ α bioassay, was also suppressed by IL‐4. Half‐maximal suppression occurred at IL‐4 concentrations between 0.02 and 0.1 ng/ml for all inflammatory cytokines. Nuclear run‐on assays showed that IL‐4 suppressed transcriptional activity of all inflammatory cytokines. Messenger RNA stability was not changed by IL‐4. The data suggest that IL‐4 plays an important transcriptional role in the regulation of alveolar macrophage inflammatory activities in respiratory disease and raise the possibility that IL‐4 may function in vivo as a coordinator of inflammatory and immune responses J. Leukoc. Biol. 56: 507–513; 1994.