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Interleukin (IL)-10 attenuates lipopolysaccharide-induced IL-6 production via inhibition of IB- activity by Bcl-3

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan, yokochi{at}aichi-med-u.ac.jp

Yoshikazu Naiki

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Gantsetseg Tumurkhuu

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Abu Shadat Mohammod Noman

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Imtiaz Iftekar-E-Khuda

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Naoki Koide

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Takayuki Komatsu

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Takashi Yokochi

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

The inhibitory effect of interleukin-10 (IL-10), an anti-inflammatory cytokine, on lipopolysaccharide (LPS)-induced IL-6 production was characterized by simultaneous stimulation of RAW 264.7 cells with LPS and IL-10. The presence of IL-10 significantly inhibited LPS-induced IL-6 production at a transcriptional level. The expression of IB-, which promotes IL-6 production, was induced in response to LPS and it was definitely suppressed in the presence of IL-10. Further, IL-10 inhibited LPS-induced NF-B activation. A pharmacological inhibitor of NF-B prevented LPS-induced IB- expression, suggesting that IL-10 might inhibit LPS-induced IB- expression via the inactivation of NF-B. In LPS- and IL-10-stimulated cells, the expression of Bcl-3 that inhibits NF-B activation was significantly augmented. Introduction of Bcl-3 siRNA abolished IL-10-mediated IB- inhibition. In the presence of Bcl-3, siRNA IL-10 failed to inhibit LPS-induced IL-6 production. Therefore, it was suggested that Bcl-3 induced by IL-10 might reduce LPS-induced IB- activity via inactivation of NF-B and that reduced IB- activity failed to promote LPS-induced IL-6 production.

Key Words: Bcl-3 • IL-10 • IL-6 • LPS • IB-

This version was published on August 1, 2009

Innate Immunity, Vol. 15, No. 4, 217-224 (2009)
DOI: 10.1177/1753425909103738


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