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MicroRNA‐98 negatively regulates IL‐10 production and endotoxin tolerance in macrophages after LPS stimulation
Author(s) -
Liu Yang,
Chen Qingyun,
Song Yinjing,
Lai Lihua,
Wang Jianli,
Yu Hai,
Cao Xuetao,
Wang Qingqing
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.05.029
Subject(s) - tlr4 , lipopolysaccharide , microrna , stimulation , microbiology and biotechnology , cytokine , downregulation and upregulation , interleukin , untranslated region , inflammation , chemistry , biology , interleukin 10 , immunology , messenger rna , signal transduction , gene , endocrinology , biochemistry
Interleukin 10 (IL‐10) is a potent anti‐inflammatory cytokine that is crucial for dampening the inflammatory response after pathogen invasion, and was found to be produced by macrophages after exposure to lipopolysaccharide (LPS). It remains unclear whether microRNA‐mediated regulatory mechanism is involved in LPS‐induced IL‐10 production. Here we reported that miR‐98 expression in macrophages significantly decreased following LPS stimulation. We also found that miR‐98 targets the 3'untranslated region of IL‐10 transcript. Overexpression of miR‐98 inhibited TLR4‐triggered IL‐10 production and promoted COX‐2 expression. We further demonstrated that miR‐98 significantly mitigated the induction of endotoxin tolerance, suggesting that miR‐98‐mediated posttranscriptional control could potentially be involved in fine tuning the critical level of IL‐10 production in endotoxin tolerance.