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Co-Culture of Murine Small Intestine Epithelial Organoids with Innate Lymphoid Cells
Published on: March 23, 2022
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Innate lymphoid cells regulate intestinal epithelial cell glycosylation
Yoshiyuki Goto1, Takashi Obata2, Jun Kunisawa3
1Division of Mucosal Immunology, Department of Microbiology and Immunology, The Institute of Medical Science, The University of Tokyo, Tokyo 108-8639, Japan. Core Research for Evolutional Science and Technology, Japan Science and Technology Agency, Saitama 332-0012, Japan. Microbe Division/Japan Collection of Microorganisms, RIKEN BioResource Center, Tsukuba 305-0074, Japan.
Science (New York, N.Y.)
|September 13, 2014
Summary
Type 3 innate lymphoid cells (ILC3) regulate gut fucosylation, a key process in host-microbiota symbiosis. This discovery reveals how ILC3s influence the gut environment and impact susceptibility to bacterial infections.
Area of Science:
- Immunology
- Microbiology
- Glycobiology
Background:
- Fucosylation of intestinal epithelial cells, catalyzed by fucosyltransferase 2 (Fut2), is crucial for host-microbiota symbiosis.
- Epithelial fucose serves as a dietary carbohydrate for commensal bacteria, but the mechanisms regulating its induction are unknown.
Purpose of the Study:
- To investigate the molecular and cellular mechanisms that regulate the induction of intestinal epithelial fucosylation.
- To identify immune cells involved in controlling epithelial glycosylation and its impact on gut homeostasis.
Main Methods:
- Studies were conducted in mouse models.
- Investigated the role of type 3 innate lymphoid cells (ILC3) in regulating Fut2 expression and fucosylation.
- Utilized cytokine neutralization (interleukin-22 and lymphotoxin) and bacterial infection models (Salmonella typhimurium).
Main Results:
- Type 3 innate lymphoid cells (ILC3) were found to induce intestinal epithelial Fut2 expression and fucosylation in mice.
- This induction was dependent on interleukin-22 (in a bacteria-dependent manner) and lymphotoxin (in a bacteria-independent manner).
- Disruption of intestinal fucosylation resulted in increased susceptibility to Salmonella typhimurium infection.
Conclusions:
- Type 3 innate lymphoid cells (ILC3) play a significant role in shaping the gut microenvironment.
- ILC3s regulate epithelial glycosylation through mechanisms involving interleukin-22 and lymphotoxin.
- Epithelial fucosylation is important for maintaining host defense against enteric pathogens like Salmonella typhimurium.
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