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The disruption of intestinal homeostasis when foods are colored red

Cellular & Molecular Immunology volume 19, pages 855–857 (2022)Cite this article

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Food colorant Red 40 has been shown to induce colitis in the context of dysregulated IL-23. However, the mechanism involved is still not fully understood. A study by Chen et al. in this issue of Cellular Molecular Immunology [1] demonstrates that under dysregulated IL-23 production from myeloid cells, Red 40 induces IFNγ+ cytotoxic CD4+ T cells to promote colitis.

It is well established that the pathogenesis of inflammatory bowel diseases (IBD) involves dysregulated mucosal immune responses to gut microbiota in genetically susceptible individuals [2]. Over 200 risk loci for IBD have been identified by genome-wide association studies (GWAS), and some of these risk loci have been evaluated in various animal models of colitis [3]. However, the combination of all these genes/loci only accounts for a small proportion of disease heritability, suggesting that environmental factors also play a critical role in the pathogenesis of IBD. Accumulating evidence has revealed that various immune cell types coordinate their functions through cytokine-mediated intercellular communication to regulate the pathogenesis of IBD [4]. IL-23 is a heterodimer that is comprised of IL12p40 and IL23p19. It is primarily produced by innate myeloid cells and acts on Th17 cells, which are crucial in mediating the pathogenesis of IBD [5]. The coding variants in IL23R are associated with protection from IBD onset, and the IL12B locus, which encodes IL-12p40, is associated with IBD risk [6]. However, overexpression of IL-23 alone in myeloid cells does not cause colitis in animal models, indicating that other factors, including local environmental variables, coordinate disease development.

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References

  1. Chen L, He Z, Reis BS, Gelles JD, Chipuk JE, Ting AT, et al. IFNγ+ cytotoxic CD4+ T lymphocytes are involved in the pathogenesis of colitis induced by IL-23 and food colorant Red 40. Cell Mol Immunol. 2022;19:777–90.

    Google Scholar 

  2. Elson CO, Cong Y. Host-microbiota interactions in inflammatory bowel disease. Gut Microbes. 2012;3:332–44.

    Article  Google Scholar 

  3. Huang H, Fang M, Jostins L, Umicevic Mirkov M, Boucher G, Anderson CA, et al. Fine-mapping inflammatory bowel disease loci to single-variant resolution. Nature. 2017;547:173–8.

    Article  CAS  Google Scholar 

  4. Bamias G, Cominelli F. Cytokines and intestinal inflammation. Curr Opin Gastroenterol. 2016;32:437–42.

    Article  CAS  Google Scholar 

  5. Cua DJ, Sherlock J, Chen Y, Murphy CA, Joyce B, Seymour B, et al. Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature. 2003;421:744–8.

    Article  CAS  Google Scholar 

  6. Duerr RH, Taylor KD, Brant SR, Rioux JD, Silverberg MS, Daly MJ, et al. A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science. 2006;314:1461–3.

    Article  CAS  Google Scholar 

  7. Lee D, Albenberg L, Compher C, Baldassano R, Piccoli D, Lewis JD, et al. Diet in the pathogenesis and treatment of inflammatory bowel diseases. Gastroenterology. 2015;148:1087–106.

    Article  CAS  Google Scholar 

  8. Vojdani A, Vojdani C. Immune reactivity to food coloring. Alter Ther Health Med. 2015;21:52–62.

    Google Scholar 

  9. Chen L, He Z, Iuga AC, Martins Filho SN, Faith JJ, Clemente JC, et al. Diet modifies colonic microbiota and CD4(+) T-cell repertoire to induce flares of colitis in mice with myeloid-cell expression of interleukin 23. Gastroenterology. 2018;155:1177–1191. e1116

    Article  CAS  Google Scholar 

  10. He Z, Chen L, Catalan-Dibene J, Bongers G, Faith JJ, Suebsuwong C, et al. Food colorants metabolized by commensal bacteria promote colitis in mice with dysregulated expression of interleukin-23. Cell Metab. 2021;33:1358–1371. e1355

    Article  CAS  Google Scholar 

  11. Globig AM, Hennecke N, Martin B, Seidl M, Ruf G, Hasselblatt P, et al. Comprehensive intestinal T helper cell profiling reveals specific accumulation of IFN-gamma+IL-17+coproducing CD4+ T cells in active inflammatory bowel disease. Inflamm Bowel Dis. 2014;20:2321–9.

    Article  Google Scholar 

  12. Allaire JM, Crowley SM, Law HT, Chang SY, Ko HJ, Vallance BA. The intestinal epithelium: central coordinator of mucosal immunity. Trends Immunol. 2018;39:677–96.

    Article  CAS  Google Scholar 

Download references

Acknowledgements

This work was supported by NIH grants DK112436, DK125011, AI150210, and DK124132. Figure 1 was created with BioRender.com.

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  1. Department of Microbiology and Immunology, The University of Texas Medical Branch, Galveston, TX, 77555, USA

    Wenjing Yang & Yingzi Cong

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  1. Wenjing Yang
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Correspondence to Yingzi Cong.

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Yang, W., Cong, Y. The disruption of intestinal homeostasis when foods are colored red. Cell Mol Immunol 19, 855–857 (2022). https://doi.org/10.1038/s41423-022-00875-0

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