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• Amini, Salah Edden; Bresson, Sophie Emilie & Ruzzin, Jerome Nicolas Marius (2023). Mice lacking intestinal Nr1i2 have normal intestinal homeostasis under steady-state conditions and are not hypersensitive to inflammation under lipopolysaccharide treatment. The FASEB Journal. ISSN 0892-6638. 37(8). doi: 10.1096/fj.202301126. Full text in Research Archive Show summary

  Abstract Nr1i2 , a nuclear receptor known for its key function in xenobiotic detoxification, has emerged as a potential regulator of intestinal homeostasis and inflammation. However, the role of Nr1i2 in different intestinal segments remains poorly known. Moreover, in vivo investigations on intestinal Nr1i2 have essentially been performed in whole‐body Nr1i2 knockout ( Nr1i2 −/− ) mice where the deletion of Nr1i2 in all tissues may affect the intestinal phenotype. To better understand the role of Nr1i2 in the intestine, we generated intestinal epithelial‐specific Nr1i2 knockout (i Nr1i2 −/− ) mice and studied the duodenum, jejunum, ileum, and colon of these animals during steady‐state conditions and lipopolysaccharide (LPS)‐induced inflammation. As compared to control (i Nr1i2 +/+ ) mice, i Nr1i2 −/− mice showed normal intestinal permeability as assessed by in vivo FITC‐dextran test. The expression of genes involved in inflammation, tight‐ and adherens‐junction, proliferation, glucose, and lipid metabolism was comparable in the duodenum, jejunum, ileum, and colon of i Nr1i2 −/− and i Nr1i2 +/+ mice. In line with these findings, histological analyses of the jejunum revealed no difference between i Nr1i2 −/− and i Nr1i2 +/+ mice. When treated with LPS, the intestine of i Nr1i2 −/− mice had no increased inflammatory response as compared to i Nr1i2 +/+ mice. Moreover, the health monitoring of LPS‐treated i Nr1i2 −/− and i Nr1i2 +/+ mice was similar. Taken together, our results demonstrate that the specific deletion of Nr1i2 in the intestinal epithelium does not cause major intestinal damages in mice during both steady‐state and inflammatory conditions.

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