ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015
Targeted 25-hydroxyvitamin D3 1α-hydroxylase adoptive gene therapy ameliorates dss-induced colitis without causing hypercalcemia in mice.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Role of Cytochromes P450 in Intestinal Barrier Function: Possible Involvement in the Pathogenesis of Leaky Gut Syndrome.Digestive diseases and sciences · 2025Review
- Therapeutic Efficacy and Underlying Mechanisms of a Mannoglucan fromInternational journal of molecular sciences · 2024Article
- Article
- Genetically modified macrophages accelerate myelin repair.EMBO molecular medicine · 2022Article
- Inflammation- and Gut-Homing Macrophages, Engineered toInternational journal of molecular sciences · 2021Article
- Low Circulating Vitamin D in Intensive Care Unit-Admitted COVID-19 Patients as a Predictor of Negative Outcomes.The Journal of nutrition · 2021Observational
- Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review.Molecules (Basel, Switzerland) · 2020Review
- Vitamin D as a Potential Therapy for Multiple Sclerosis: Where Are We?International journal of molecular sciences · 2020Review
- Mechanistic study of the cause of decreased blood 1,25-Dihydroxyvitamin D in sepsis.BMC infectious diseases · 2019Observational
- In Vivo Generation of Gut-Homing Regulatory T Cells for the Suppression of Colitis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- 1,25-Dihydroxyvitamin D suppresses M1 macrophages and promotes M2 differentiation at bone injury sites.JCI insight · 2018Article
- Deficient arginase II expression without alteration in arginase I expression attenuated experimental autoimmune encephalomyelitis in mice.Immunology · 2018Article
- Physiologic and pathophysiologic roles of extra renal CYP27b1: Case report and review.Bone reports · 2018Article
- Dendritic cells, engineered to overexpress 25-hydroxyvitamin D 1α-hydroxylase and pulsed with a myelin antigen, provide myelin-specific suppression of ongoing experimental allergic encephalomyelitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Disequilibrium in the CD8Digestive diseases and sciences · 2017Article
- MicroRNA223 promotes pathogenic T-cell development and autoimmune inflammation in central nervous system in mice.Immunology · 2016Article
- Protective links between vitamin D, inflammatory bowel disease and colon cancer.World journal of gastroenterology · 2016Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic 1,25(OH)2D3 treatment ameliorating murine inflammatory bowel diseases (IBD) could not be applied to patients because of hypercalcemia. We tested the hypothesis that increasing 1,25(OH)2D3 synthesis locally by targeting delivery of the 1α-hydroxylase gene (CYP27B1) to the inflamed bowel would ameliorate IBD without causing hypercalcemia. Our targeting strategy is the use of CD11b(+)/Gr1(+) monocytes as the cell vehicle and a macrophage-specific promoter (Mac1) to control CYP27B1 expression. The CD11b(+)/Gr1(+) monocytes migrated initially to inflamed colon and some healthy tissues in dextran sulfate sodium (DSS) colitis mice; however, only the migration of monocytes to the inflamed colon was sustained. Adoptive transfer of Gr1(+) monocytes did not cause hepatic injury. Infusion of Mac1-CYP27B1-modified monocytes increased body weight gain, survival, and colon length, and expedited mucosal regeneration. Expression of pathogenic Th17 and Th1 cytokines (interleukin (IL)-17a and interferon (IFN)-α) was decreased, while expression of protective Th2 cytokines (IL-5 and IL-13) was increased, by the treatment. This therapy also enhanced tight junction gene expression in the colon. No hypercalcemia occurred following this therapy. In conclusion, we have for the first time obtained proof-of-principle evidence for a novel monocyte-based adoptive CYP27B1 gene therapy using a mouse IBD model. This strategy could be developed into a novel therapy for IBD and other autoimmune diseases.
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