ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Active vitamin D (1,25-dihydroxyvitamin D3) increases host susceptibility to Citrobacter rodentium by suppressing mucosal Th17 responses.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Interactions between Dietary Antioxidants, Dietary Fiber and the Gut Microbiome: Their Putative Role in Inflammation and Cancer.International journal of molecular sciences · 2024Review
- Gut microbiota in pathophysiology, diagnosis, and therapeutics of inflammatory bowel disease.Intestinal research · 2024Review
- Review
- Role of vitamin D in regulating COVID-19 severity-An immunological perspective.Journal of leukocyte biology · 2021Review
- Role of Food Antioxidants in Modulating Gut Microbial Communities: Novel Understandings in Intestinal Oxidative Stress Damage and Their Impact on Host Health.Antioxidants (Basel, Switzerland) · 2021Review
- Effects of Vitamin D-Deficient Diet on Intestinal Epithelial Integrity and Zonulin Expression in a C57BL/6 Mouse Model.Frontiers in medicine · 2021Article
- Vitamin D and Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD): An Update.Nutrients · 2020Review
- Intestinal Macrophages at the Crossroad between Diet, Inflammation, and Cancer.International journal of molecular sciences · 2020Review
- Peripheral and Central Nervous System Immune Response Crosstalk in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2020Review
- Conceptual Development of Immunotherapeutic Approaches to Gastrointestinal Cancer.International journal of molecular sciences · 2019Review
- Current evidence for vitamin D in intestinal function and disease.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- Vitamin D/Vitamin D Receptor Signaling Is Required for Normal Development and Function of Group 3 Innate Lymphoid Cells in the Gut.iScience · 2019Article
- Aligning the Paradoxical Role of Vitamin D in Gastrointestinal Immunity.Trends in endocrinology and metabolism: TEM · 2019Review
- Vitamin A and vitamin D regulate the microbial complexity, barrier function, and the mucosal immune responses to ensure intestinal homeostasis.Critical reviews in biochemistry and molecular biology · 2019Review
- Vitamin D Is Required for ILC3 Derived IL-22 and Protection FromFrontiers in immunology · 2019Article
- Inflammatory bowel disease and immunonutrition: novel therapeutic approaches through modulation of diet and the gut microbiome.Immunology · 2018Review
- Vitamin D and Influenza-Prevention or Therapy?International journal of molecular sciences · 2018Review
- Article
- Dysbiosis of gut microbiota in promoting the development of colorectal cancer.Gastroenterology report · 2018Review
- Influence of Microbiota on Intestinal Immune System in Ulcerative Colitis and Its Intervention.Frontiers in immunology · 2017Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Vitamin D deficiency affects more that 1 billion people worldwide and is associated with an increased risk of developing a number of inflammatory/autoimmune diseases, including inflammatory bowel disease (IBD). At present, the basis for the impact of vitamin D on IBD and mucosal immune responses is unclear; however, IBD is known to reflect exaggerated immune responses to luminal bacteria, and vitamin D has been shown to play a role in regulating bacteria-host interactions. Therefore, to test the effect of active vitamin D on host responses to enteric bacteria, we gave 1,25(OH)(2)D(3) to mice infected with the bacterial pathogen Citrobacter rodentium, an extracellular microbe that causes acute colitis characterized by a strong Th1/Th17 immune response. 1,25(OH)(2)D(3) treatment of infected mice led to increased pathogen burdens and exaggerated tissue pathology. In association with their increased susceptibility, 1,25(OH)(2)D(3)-treated mice showed substantially reduced numbers of Th17 T cells within their infected colons, whereas only modest differences were noted in Th1 and Treg numbers. In accordance with the impaired Th17 responses, 1,25(OH)(2)D(3)-treated mice showed defects in their production of the antimicrobial peptide REG3γ. Taken together, these studies show that 1,25(OH)(2)D(3) suppresses Th17 T-cell responses in vivo and impairs mucosal host defense against an enteric bacterial pathogen.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.