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B Protein IBNS Selectively Inhibits Lipopolysaccharide-Induced IL-6 Production in Macrophages of the Colonic Lamina Propria 1
* Department of Host Defense, Research Institute for Microbial Diseases and
Department of Molecular Medicine, Graduate School of Medicine, Osaka University, and
Exploratory Research for Advanced Technology, Japan Science and Technology Agency, Osaka, Japan;
Department of Molecular Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan; and
¶ Department of Medicine, Division of Rheumatology and Clinical Immunology, University of Florida, Gainesville, FL 32610
Macrophages play an important role in the pathogenesis of chronic colitis. However, it remains unknown how macrophages residing in the colonic lamina propria are regulated. We characterized colonic lamina proprial CD11b-positive cells (CLPM
). CLPM of wild-type mice, but not IL-10-deficient mice, displayed hyporesponsiveness to TLR stimulation in terms of cytokine production and costimulatory molecule expression. We compared CLPM gene expression profiles of wild-type mice with IL-10-deficient mice, and identified genes that are selectively expressed in wild-type CLPM. These genes included nuclear I
B proteins such as Bcl-3 and IBNS. Because Bcl-3 has been shown to specifically inhibit LPS-induced TNF-
production, we analyzed the role of IBNS in macrophages. Lentiviral introduction of IBNS resulted in impaired LPS-induced IL-6 production, but not TNF- production in the murine macrophage cell line RAW264.7. IBNS expression led to constitutive and intense DNA binding of NF-B p50/p50 homodimers. IBNS was recruited to the IL-6 promoter, but not to the TNF- promoter, together with p50. Furthermore, small interference RNA-mediated reduction in IBNS expression in RAW264.7 cells resulted in increased LPS-induced production of IL-6, but not TNF-. Thus, IBNS selectively suppresses LPS-induced IL-6 production in macrophages. This study established that nuclear IB proteins differentially regulate LPS-induced inflammatory cytokine production in macrophages.
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