Suppression of TNFα expression induced by indole-3-acetic acid is not mediated by AhR activation in Caco-2 cells

Md Mazharul Islam Chowdhury; Koichi Kurata; Kana Yuasa; Yoshihito Koto; Kohji Nishimura; Hidehisa Shimizu

doi:10.1093/bbb/zbaa101

Suppression of TNFα expression induced by indole-3-acetic acid is not mediated by AhR activation in Caco-2 cells

Biosci Biotechnol Biochem. 2021 Mar 24;85(4):902-906. doi: 10.1093/bbb/zbaa101.

Authors

Md Mazharul Islam Chowdhury¹, Koichi Kurata², Kana Yuasa³, Yoshihito Koto³, Kohji Nishimura^{1

2

3

4

5

6}, Hidehisa Shimizu^{1

2

3

4

5

6

7

8}

Affiliations

¹ The United Graduate School of Agricultural Sciences, Tottori University, Tottori-Shi, Tottori, Japan.
² Graduate School of Life and Environmental Science, Shimane University, Matsue, Shimane, Japan.
³ Graduate School of Natural Science and Technology, Shimane University, Matsue, Shimane, Japan.
⁴ Raman Project Center for Medical and Biological Applications, Shimane University, Matsue, Shimane, Japan.
⁵ Interdisciplinary Center for Science Research, Shimane University, Matsue, Shimane, Japan.
⁶ Institute of Agricultural and Life Sciences, Academic Assembly, Shimane University, Matsue, Shimane, Japan.
⁷ Estuary Research Center, Shimane University, Matsue, Shimane, Japan.
⁸ Project Center for Fortification of Local Specialty Food Functions, Shimane University, Matsue, Shimane, Japan.

PMID: 33580679
DOI: 10.1093/bbb/zbaa101

Abstract

Indole-3-acetic acid (IAA) produced by intestinal bacteria from tryptophan in dietary proteins is considered to suppress the inflammatory response through aryl hydrocarbon receptor (AhR) activation. However, AhR activation was not involved in the downregulation of tumor necrosis factor α (TNFα) expression induced by IAA in Caco-2 cells. The activation of unidentified IAA receptors might attenuate the inflammatory response to TNFα in colorectal cancer cells.

Keywords: aryl hydrocarbon receptor; colorectal cancer; cytochrome P450 1A1; inflammation; tumor necrosis factor α.

MeSH terms

Caco-2 Cells
Humans
Indoleacetic Acids / metabolism*
Inflammation / genetics
Receptors, Aryl Hydrocarbon / metabolism*
Tumor Necrosis Factor-alpha / genetics*

Substances

Indoleacetic Acids
Receptors, Aryl Hydrocarbon
Tumor Necrosis Factor-alpha
indoleacetic acid