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Cited by 167NF-κB Signaling PathwaysImmune Response and InflammationInflammatory Bowel Disease

The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.

The Nuclear IκB Protein IκBNS Selectively Inhibits Lipopolysaccharide-Induced IL-6 Production in Macrophages of the Colonic Lamina Propria

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Hirotani, Tomonori, Lee, Pui Y, Kuwata, Hirotaka, Yamamoto, Masahiro, Matsumoto, Makoto, Kawase, Ichiro, Akira, Shizuo, Takeda, Kiyoshi·2005·The Journal of Immunology
DOI 10.4049/jimmunol.174.6.3650
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Abstract

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 (CLPMφ). CLPMφ 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 CLPMφ gene expression profiles of wild-type mice with IL-10-deficient mice, and identified genes that are selectively expressed in wild-type CLPMφ. These genes included nuclear IκB proteins such as Bcl-3 and IκBNS. Because Bcl-3 has been shown to specifically inhibit LPS-induced TNF-α production, we analyzed the role of IκBNS in macrophages. Lentiviral introduction of IκBNS resulted in impaired LPS-induced IL-6 production, but not TNF-α production in the murine macrophage cell line RAW264.7. IκBNS expression led to constitutive and intense DNA binding of NF-κB p50/p50 homodimers. IκBNS was recruited to the IL-6 promoter, but not to the TNF-α promoter, together with p50. Furthermore, small interference RNA-mediated reduction in IκBNS expression in RAW264.7 cells resulted in increased LPS-induced production of IL-6, but not TNF-α. Thus, IκBNS selectively suppresses LPS-induced IL-6 production in macrophages. This study established that nuclear IκB proteins differentially regulate LPS-induced inflammatory cytokine production in macrophages.

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Metadata

Authors
Hirotani, T., Lee, P. Y., Kuwata, H., Yamamoto, M., Matsumoto, M., Kawase, I., Akira, S., & Takeda, K.
Affiliations
  • Research Institute for Microbial Diseases, The University of Osaka (JP)
  • University of Florida Health (US)
  • Kyushu University (JP)
  • Japan Science and Technology Agency (JP)
  • The University of Osaka (JP)
Corresponding author
  • Hirotani, Tomonori
  • Yamamoto, Masahiro
  • Akira, Shizuo
ORCID
Venue
The Journal of Immunology
Publisher
Oxford University Press (OUP)
Published
2005-03
Volume
174
Issue
6
Pages
3650-3657
ISSN
  • 0022-1767 (ISSN-L)
  • 1550-6606
DOI
10.4049/jimmunol.174.6.3650
OpenAlex
W1503222294
Cited by
167
References
42
Citations by year
2025: 3 · 2024: 1 · 2023: 3 · 2022: 5 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 15 · 2016: 8 · 2015: 8 · 2014: 10 · 2013: 8 · 2012: 11
FWCI
3.95
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • The Journal of Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
Ministry of Education, Culture, Sports, Science and Technology
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
Keywords
Bcl-3, interleukin-6, TNF-α, lipopolysaccharide, macrophages, colonic lamina propria, IL-10, Toll-like receptor signaling, chronic colitis, IL-6 promoter
MeSH terms
Animals, Base Sequence, Cell Line, Colon, DNA, Humans, Intestinal Mucosa, Lipopolysaccharides, Macrophages, Mice, Inbred C57BL, Promoter Regions, Genetic, Protein Precursors, Proteins, Recombinant Proteins, Tumor Necrosis Factor-alpha, Interleukin-6, Gene Expression, NF-kappa B, Mice, Knockout, CD11b Antigen, Intracellular Signaling Peptides and Proteins, Mice, NF-kappa B p50 Subunit, In Vitro Techniques

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