Key studies published in 2019 highlight novel concepts regarding the pathogenesis of inflammatory bowel disease: the emerging role of host–microorganism interactions and the regional microbiota as disease drivers, and the identification of new therapeutic targets. These findings suggest new avenues for research and define important hallmarks for clinical diagnosis and therapy.
Key advances
Specific microbial pathways control intestinal epithelial cell and barrier function and determine responsiveness to anti-TNF therapy, suggesting that targeting of these pathways is relevant for inflammatory bowel disease (IBD) therapy3; increased Bifidobacterium, Collinsella, Lachnospira, Lachnospiraceae, Roseburia and Eggerthella taxa are related to successful outcome (clinical response or remission) of anti-TNF therapy in Crohn’s disease.
Many defined microbial metabolites are depleted in individuals with IBD versus control individuals, indicating that loss of metabolic diversity occurs with dysbiosis and loss of taxonomic diversity in the IBD microbiome4.
The transcription factor c-MAF is a key factor in gut regulatory T cells that maintains host–microorganism homeostasis and prevents gut inflammation5.
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References
Sands, B. E. et al. Ustekinumab as induction and maintenance therapy for ulcerative colitis. N. Engl. J. Med. 381, 1201–1214 (2019).
Neurath, M. F. Targeting immune cell circuits and trafficking in inflammatory bowel disease. Nat. Immunol. 20, 970–979 (2019).
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Franzosa, E. A. et al. Gut microbiome structure and metabolic activity in inflammatory bowel disease. Nat. Microbiol. 4, 293–305 (2019).
Neumann, C. et al. c-Maf-dependent Treg cell control of intestinal TH17 cells and IgA establishes host-microbiota homeostasis. Nat. Immunol. 20, 471–481 (2019).
Arpaia, N. et al. Metabolites produced by commensal bacteria promote peripheral regulatory T cell generation. Nature 504, 451–455 (2013).
Furusawa, Y. et al. Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells. Nature 504, 446–450 (2013).
Sujino, T. et al. Regulatory T cells suppress development of colitis, blocking differentiation of T-helper 17 into alternative T-helper 1 cells. Gastroenterology 141, 1014–023 (2011).
Maul, J. et al. Peripheral and intestinal regulatory CD4+ CD25(high) T cells in inflammatory bowel disease. Gastroenterology 128, 1868–1878 (2005).
Zundler, S. et al. Hobit- and Blimp-1-driven CD4+ tissue-resident memory T cells control chronic intestinal inflammation. Nat. Immunol. 20, 288–300 (2019).
Acknowledgements
M.F.N. is supported by the Clinical Research Group 257 CEDER, the SFB1181, the TRR241, the FOR2438 of the Deutsche Forschungsgemeinschaft, the Interdisciplinary Center for Clinical Research (IZKF) and the Emerging Fields Initiative of the Friedrich Alexander Universität Erlangen-Nürnberg.
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M.F.N. has served as an adviser or received research grants from Abbvie, Amgen, Boehringer, Janssen, MSD, Pentax, Pfizer, PPM, Roche and Takeda.
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Neurath, M.F. Host–microbiota interactions in inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 17, 76–77 (2020). https://doi.org/10.1038/s41575-019-0248-1
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DOI: https://doi.org/10.1038/s41575-019-0248-1
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