Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis

Tomoki Sasaki; Hiroyuki Nagashima; Atsushi Okuma; Takeshi Yamauchi; Kenshi Yamasaki; Setsuya Aiba; Takanori So; Naoto Ishii; Yuji Owada; Takashi MaruYama; Shuhei Kobayashi

doi:10.1007/s10620-021-06958-8

Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis

Tomoki Sasaki, Hiroyuki Nagashima, Atsushi Okuma, Takeshi Yamauchi, Kenshi Yamasaki, Setsuya Aiba, Takanori So, Naoto Ishii, Yuji Owada, Takashi MaruYama, Shuhei Kobayashi

MED - Medical Sciences

Research output: Contribution to journal › Article › peer-review

Abstract

Background: The Toll-like receptor signaling pathway contributes to the regulation of intestinal homeostasis through interactions with commensal bacteria. Although the transcriptional regulator IκB-ζ can be induced by Toll-like receptor signaling, its role in intestinal homeostasis is still unclear. Aims: To investigate the role of IκB-ζ in gut homeostasis. Methods: DSS-administration induced colitis in control and IκB-ζ-deficient mice. The level of immunoglobulins in feces was detected by ELISA. The immunological population in lamina propria (LP) was analyzed by FACS. Results: IκB-ζ-deficient mice showed severe inflammatory diseases with DSS administration in the gut. The level of IgM in the feces after DSS administration was less in IκB-ζ-deficient mice compared to control mice. Upon administration of DSS, IκB-ζ-deficient mice showed exaggerated intestinal inflammation (more IFN-g-producing CD4⁺ T cells in LP), and antibiotic treatment canceled this inflammatory phenotype. Conclusion: IκB-ζ plays a crucial role in maintaining homeostasis in the gut.

Original language	English
Pages (from-to)	1252-1259
Number of pages	8
Journal	Digestive Diseases and Sciences
Volume	67
Issue number	4
DOIs	https://doi.org/10.1007/s10620-021-06958-8
Publication status	Published - 2022 Apr

Keywords

Gut homeostasis
Inflammatory bowel disease (IBD)
IκB-ζ

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10.1007/s10620-021-06958-8

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title = "Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis",

abstract = "Background: The Toll-like receptor signaling pathway contributes to the regulation of intestinal homeostasis through interactions with commensal bacteria. Although the transcriptional regulator IκB-ζ can be induced by Toll-like receptor signaling, its role in intestinal homeostasis is still unclear. Aims: To investigate the role of IκB-ζ in gut homeostasis. Methods: DSS-administration induced colitis in control and IκB-ζ-deficient mice. The level of immunoglobulins in feces was detected by ELISA. The immunological population in lamina propria (LP) was analyzed by FACS. Results: IκB-ζ-deficient mice showed severe inflammatory diseases with DSS administration in the gut. The level of IgM in the feces after DSS administration was less in IκB-ζ-deficient mice compared to control mice. Upon administration of DSS, IκB-ζ-deficient mice showed exaggerated intestinal inflammation (more IFN-g-producing CD4+ T cells in LP), and antibiotic treatment canceled this inflammatory phenotype. Conclusion: IκB-ζ plays a crucial role in maintaining homeostasis in the gut.",

keywords = "Gut homeostasis, Inflammatory bowel disease (IBD), IκB-ζ",

author = "Tomoki Sasaki and Hiroyuki Nagashima and Atsushi Okuma and Takeshi Yamauchi and Kenshi Yamasaki and Setsuya Aiba and Takanori So and Naoto Ishii and Yuji Owada and Takashi MaruYama and Shuhei Kobayashi",

note = "Funding Information: We are grateful to Dr. Tatsushi Muta (Tohoku University) [44] for providing critical materials and discussion. Histological scoring was performed by ALLISERE Co. Ltd. (Tokyo, Japan). Funding Information: This work was supported by a Grant-in-Aid for challenging Exploratory Research [Grant Numbers 26670019] from the Japan Society for the Promotion of Science to T.M.Y. Publisher Copyright: {\textcopyright} 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.",

year = "2022",

month = apr,

doi = "10.1007/s10620-021-06958-8",

language = "English",

volume = "67",

pages = "1252--1259",

journal = "Digestive Diseases and Sciences",

issn = "0163-2116",

publisher = "Springer New York",

number = "4",

}

TY - JOUR

T1 - Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis

AU - Sasaki, Tomoki

AU - Nagashima, Hiroyuki

AU - Okuma, Atsushi

AU - Yamauchi, Takeshi

AU - Yamasaki, Kenshi

AU - Aiba, Setsuya

AU - So, Takanori

AU - Ishii, Naoto

AU - Owada, Yuji

AU - MaruYama, Takashi

AU - Kobayashi, Shuhei

N1 - Funding Information: We are grateful to Dr. Tatsushi Muta (Tohoku University) [44] for providing critical materials and discussion. Histological scoring was performed by ALLISERE Co. Ltd. (Tokyo, Japan). Funding Information: This work was supported by a Grant-in-Aid for challenging Exploratory Research [Grant Numbers 26670019] from the Japan Society for the Promotion of Science to T.M.Y. Publisher Copyright: © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

PY - 2022/4

Y1 - 2022/4

N2 - Background: The Toll-like receptor signaling pathway contributes to the regulation of intestinal homeostasis through interactions with commensal bacteria. Although the transcriptional regulator IκB-ζ can be induced by Toll-like receptor signaling, its role in intestinal homeostasis is still unclear. Aims: To investigate the role of IκB-ζ in gut homeostasis. Methods: DSS-administration induced colitis in control and IκB-ζ-deficient mice. The level of immunoglobulins in feces was detected by ELISA. The immunological population in lamina propria (LP) was analyzed by FACS. Results: IκB-ζ-deficient mice showed severe inflammatory diseases with DSS administration in the gut. The level of IgM in the feces after DSS administration was less in IκB-ζ-deficient mice compared to control mice. Upon administration of DSS, IκB-ζ-deficient mice showed exaggerated intestinal inflammation (more IFN-g-producing CD4+ T cells in LP), and antibiotic treatment canceled this inflammatory phenotype. Conclusion: IκB-ζ plays a crucial role in maintaining homeostasis in the gut.

AB - Background: The Toll-like receptor signaling pathway contributes to the regulation of intestinal homeostasis through interactions with commensal bacteria. Although the transcriptional regulator IκB-ζ can be induced by Toll-like receptor signaling, its role in intestinal homeostasis is still unclear. Aims: To investigate the role of IκB-ζ in gut homeostasis. Methods: DSS-administration induced colitis in control and IκB-ζ-deficient mice. The level of immunoglobulins in feces was detected by ELISA. The immunological population in lamina propria (LP) was analyzed by FACS. Results: IκB-ζ-deficient mice showed severe inflammatory diseases with DSS administration in the gut. The level of IgM in the feces after DSS administration was less in IκB-ζ-deficient mice compared to control mice. Upon administration of DSS, IκB-ζ-deficient mice showed exaggerated intestinal inflammation (more IFN-g-producing CD4+ T cells in LP), and antibiotic treatment canceled this inflammatory phenotype. Conclusion: IκB-ζ plays a crucial role in maintaining homeostasis in the gut.

KW - Gut homeostasis

KW - Inflammatory bowel disease (IBD)

KW - IκB-ζ

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JO - Digestive Diseases and Sciences

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ER -

Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis

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