ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Loss of n-6 fatty acid induced pediatric obesity protects against acute murine colitis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- INVITED COMMENTARY on Andersen S, et al. Developmental Windows of Environmental Vulnerability for Inflammatory Bowel Disease.Journal of pediatrics. Clinical practice · 2024Article
- Dietary-Induced Bacterial Metabolites Reduce Inflammation and Inflammation-Associated Cancer via Vitamin D Pathway.International journal of molecular sciences · 2023Article
- Role of the CXCL13/CXCR5 Axis in Autoimmune Diseases.Frontiers in immunology · 2022Review
- Effects of Maresin 1 (MaR1) on Colonic Inflammation and Gut Dysbiosis in Diet-Induced Obese Mice.Microorganisms · 2020Article
- The Role of Long-Chain Fatty Acids in Inflammatory Bowel Disease.Mediators of inflammation · 2019Review
- Emerging Roles for Noncanonical NF-κB Signaling in the Modulation of Inflammatory Bowel Disease Pathobiology.Inflammatory bowel diseases · 2016Review
- Microbiome-Epigenome Interactions and the Environmental Origins of Inflammatory Bowel Diseases.Journal of pediatric gastroenterology and nutrition · 2016Review
- Mucosal Interactions between Genetics, Diet, and Microbiome in Inflammatory Bowel Disease.Frontiers in immunology · 2016Review
- Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Dietary influences may affect microbiome composition and host immune responses, thereby modulating propensity toward inflammatory bowel diseases (IBDs): Crohn disease (CD) and ulcerative colitis (UC). Dietary n-6 fatty acids have been associated with UC in prospective studies. However, the critical developmental period when (n-6) consumption may induce UC is not known. We examined the effects of transiently increased n-6 consumption during pediatric development on subsequent dextran-sulfate-sodium (DSS)-induced acute murine colitis. The animals transiently became obese then rapidly lost this phenotype. Interestingly, mice were protected against DSS colitis 40 days after n-6 consumption. The transient high n-6-induced protection against colitis was fat type- and dietary reversal-dependent and could be transferred to germ-free mice by fecal microbiota transplantation. We also detected decreased numbers of chemokine receptor (Cxcr)5(+) CD4(+) T cells in the mesenteric lymph nodes (MLNs) of transiently n-6-fed mice. Further experiments revealed that anti-chemokine ligand (Cxcl)13 (the ligand of Cxcr5) antibody treatment decreased DSS colitis severity, implicating the importance of the Cxcr5-Cxcl13 pathway in mammalian colitis. Consecutively, we found elevated CXCL13 concentrations (CD: 1.8-fold, P = 0.0077; UC: 1.9-fold, P = 0.056) in the serum of untreated pediatric IBD patients. The human serologic observations supported the translational relevance of our findings.
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