1,25-Dihydroxyvitamin D 3 and dietary vitamin D reduce inflammation in mice lacking intestinal epithelial cell Rab11a.

Autor: Goswami S; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Flores J; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Balasubramanian I; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Bandyopadhyay S; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Joseph I; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Bianchi-Smak J; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Dhawan P; Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, New Jersey, USA., Mücahit DM; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Yu S; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA., Christakos S; Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers, The State University of New Jersey, New Jersey Medical School, Newark, New Jersey, USA., Gao N; Department of Biological Sciences, Rutgers, The State University of New Jersey, Newark, New Jersey, USA.
Jazyk: angličtina
Zdroj: Journal of cellular physiology [J Cell Physiol] 2021 Dec; Vol. 236 (12), pp. 8148-8159. Date of Electronic Publication: 2021 Jun 30.
DOI: 10.1002/jcp.30486
Abstrakt: A number of studies have examined the effects of 1,25-dihydroxyvitamin D 3 (1,25(OH) 2 D 3 ) on intestinal inflammation driven by immune cells, while little information is currently available about its impact on inflammation caused by intestinal epithelial cell (IEC) defects. Mice lacking IEC-specific Rab11a a recycling endosome small GTPase resulted in increased epithelial cell production of inflammatory cytokines, notably IL-6 and early onset of enteritis. To determine whether vitamin D supplementation may benefit hosts with epithelial cell-originated mucosal inflammation, we evaluated in vivo effects of injected 1,25(OH) 2 D 3 or dietary supplement of a high dose of vitamin D on the gut phenotypes of IEC-specific Rab11a knockout mice (Rab11a ΔIEC ). 1,25(OH) 2 D 3 administered at 25 ng, two doses per mouse, by intraperitoneal injection, reduced inflammatory cytokine production in knockout mice compared to vehicle-injected mice. Remarkably, feeding mice with dietary vitamin D supplementation at 20,000 IU/kg spanning fetal and postnatal developmental stages led to improved bodyweights, reduced immune cell infiltration, and decreased inflammatory cytokines. We found that these vitamin D effects were accompanied by decreased NF-κB (p65) in the knockout intestinal epithelia, reduced tissue-resident macrophages, and partial restoration of epithelial morphology. Our study suggests that dietary vitamin D supplementation may prevent and limit intestinal inflammation in hosts with high susceptibility to chronic inflammation.
(© 2021 Wiley Periodicals LLC.)
Databáze: MEDLINE
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