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  11. Expression Of Free Fatty Acid Receptor 2 By Dendritic Cells Prevents Their Expression Of Interleukin 27 And Is Required For Maintenance Of Mucosal Barrier And Immune Response Against Colorectal Tumors In Mice.

Expression of Free Fatty Acid Receptor 2 by Dendritic Cells Prevents Their Expression of Interleukin 27 and Is Required for Maintenance of Mucosal Barrier and Immune Response Against Colorectal Tumors in Mice.

Sydney Lavoie1, Eunyoung Chun1, Sena Bae1

  • 1Departments of Immunology and Infectious Diseases and Genetics and Complex Diseases, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.

Gastroenterology
|January 10, 2020

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View abstract on PubMed

Summary
This summary is machine-generated.

Loss of FFAR2 promotes colorectal cancer (CRC) in mice by impairing gut barrier function and altering immune responses. Targeting IL27 or using FFAR2 agonists may offer new CRC treatments.

Area of Science:

  • Gastroenterology and Oncology
  • Immunology
  • Microbiome Research

Background:

  • Intestinal microbes and their metabolites, such as short-chain fatty acids, influence colorectal cancer (CRC) development.
  • Free fatty acid receptor 2 (FFAR2) is a receptor for short-chain fatty acids and impacts the gut microbiome composition.

Purpose of the Study:

  • To investigate the role of FFAR2 in the pathogenesis of colorectal cancer (CRC).
  • To elucidate the mechanisms by which FFAR2 influences CRC development and progression.

Main Methods:

  • Studies involved ApcMin/+ mice with varying Ffar2 gene expression, including knockout and conditional knockout models in dendritic cells (DCs).
  • Mice were subjected to induced colitis with or without FFAR2 agonist or IL27 antibody treatment.
  • Analysis included histology, gene expression (qPCR, RNA-seq), 16S rRNA sequencing, flow cytometry, and intestinal permeability assays.
Keywords:
Cytokine: CytotoxicityMicrobial Metabolite ReceptorSCFA

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Main Results:

  • Loss of FFAR2 in mice led to increased spontaneous colon tumors, heightened gut permeability, reduced E-cadherin, and increased tumor bacterial load.
  • FFAR2 deficiency resulted in higher frequencies of exhausted CD8+ T cells and activated, dying DCs producing IL27.
  • IL27 antibody treatment and FFAR2 agonist administration reduced tumor development in mouse models.

Conclusions:

  • FFAR2 deficiency promotes CRC in mice by compromising gut barrier integrity, increasing bacterial load, and promoting immune cell dysfunction (T cell exhaustion, DC overactivation/death).
  • Targeting IL27 with antibodies or utilizing FFAR2 agonists demonstrates potential therapeutic strategies for CRC treatment.