Dietary vitamin B6 intake modulates colonic inflammation in the IL10−/− model of inflammatory bowel disease

Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5’-phosphate (PLP) <20 nmol/L] is observed in 19–27% of the US population. Plasma PLP concentration...

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Veröffentlicht in:	The Journal of nutritional biochemistry Jg. 24; H. 12; S. 2138 - 2143
Hauptverfasser:	Selhub, Jacob, Byun, Alexander, Liu, Zhenhua, Mason, Joel B., Bronson, Roderick T., Crott, Jimmy W.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Elsevier Inc 01.12.2013
Schlagworte:	Animals Biomarkers - blood C-reactive protein C-Reactive Protein - metabolism chemical reactions chemotaxis Colitis Colon Colon - drug effects Colon - physiopathology Cyclooxygenase 2 - metabolism diet Dietary Supplements Disease Models, Animal Female genetic markers Helicobacter hepaticus Inflammation inflammatory bowel disease Inflammatory Bowel Diseases - drug therapy interferon-gamma Interferon-gamma - metabolism Interleukin-10 - metabolism interleukin-6 Interleukin-6 - metabolism Lysophospholipids - metabolism Male Mice Mice, Knockout Nitric Oxide Synthase Type II - metabolism pyridoxal Pyridoxal 5’ phosphate pyridoxine Shingosine 1 phosphate sphingosine Sphingosine - analogs & derivatives Sphingosine - metabolism tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - metabolism United States Vitamin B 6 - administration & dosage Vitamin B 6 - blood weanlings United States S1P PLP Pyridoxal 5’ phosphate IBD Inflammation Colitis Colon Shingosine 1 phosphate Inflammatory bowel disease Pyridoxal 5’-phosphate Sphingosine 1-phosphate
ISSN:	0955-2863, 1873-4847, 1873-4847
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Abstract	Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5’-phosphate (PLP) <20 nmol/L] is observed in 19–27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10−/− (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation.
AbstractList	Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5'-phosphate (PLP) <20 nmol/L] is observed in 19-27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10(-/-) (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation.Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5'-phosphate (PLP) <20 nmol/L] is observed in 19-27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10(-/-) (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation. Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5’-phosphate (PLP) <20 nmol/L] is observed in 19–27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10−/− (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation. Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is rare, mild inadequacy [plasma pyridoxal 5'-phosphate (PLP) <20 nmol/L] is observed in 19-27% of the US population. Plasma PLP concentrations are inversely related to markers of inflammation such as C-reactive protein. Furthermore, plasma PLP is diminished in those with inflammatory conditions and, in the case of inflammatory bowel disease (IBD), more so in those with active versus quiescent disease. Restricting B6 intake attenuates IBD pathology in mice; however, the effects of supplementation are unclear. We therefore sought to determine the effects of mild inadequacy and moderate supplementation of B6 on the severity of colonic inflammation. Weanling IL-10(-/-) (positive for Helicobacter hepaticus) mice were fed diets containing 0.5 (deficient), 6.0 (replete) or 24 (supplemented) mg/kg pyridoxine HCl for 12 weeks and then assessed for histological and molecular markers of colonic inflammation. Both low and high plasma PLP were associated with a significant suppression of molecular (TNFα, IL-6, IFN-γ, COX-2 and iNOS expression) and histological markers of inflammation in the colon. PLP is required for the breakdown of sphingosine 1-phosphate (S1P), a chemotactic lipid, by S1P lyase. Colonic concentrations of S1P and PLP were significantly and inversely correlated. If confirmed, vitamin B6 supplementation may offer an additional tool for the management of IBD. Although B6 is required in dozens of reactions, its role in the breakdown of S1P may explain the biphasic relationship observed between PLP and inflammation.
Author	Selhub, Jacob Crott, Jimmy W. Byun, Alexander Bronson, Roderick T. Liu, Zhenhua Mason, Joel B.
AuthorAffiliation	d Rodent Histopathology Core, Harvard Medical School, Boston, MA c Department of Nutrition, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA b Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA a Vitamin Metabolism, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA
AuthorAffiliation_xml	– name: c Department of Nutrition, School of Public Health and Health Sciences, University of Massachusetts, Amherst, MA – name: a Vitamin Metabolism, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA – name: d Rodent Histopathology Core, Harvard Medical School, Boston, MA – name: b Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA
Author_xml	– sequence: 1 givenname: Jacob surname: Selhub fullname: Selhub, Jacob organization: Vitamin Metabolism, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 2 givenname: Alexander surname: Byun fullname: Byun, Alexander organization: Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 3 givenname: Zhenhua surname: Liu fullname: Liu, Zhenhua organization: Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 4 givenname: Joel B. surname: Mason fullname: Mason, Joel B. organization: Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA – sequence: 5 givenname: Roderick T. surname: Bronson fullname: Bronson, Roderick T. organization: Rodent Histopathology Core, Harvard Medical School, Boston, MA – sequence: 6 givenname: Jimmy W. surname: Crott fullname: Crott, Jimmy W. email: jimmy.crott@tufts.edu organization: Vitamins and Carcinogenesis Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24183308$$D View this record in MEDLINE/PubMed
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Keywords	S1P PLP Pyridoxal 5’ phosphate IBD Inflammation Colitis Colon Shingosine 1 phosphate Inflammatory bowel disease Pyridoxal 5’-phosphate Sphingosine 1-phosphate
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Snippet	Pyridoxal-5-phosphate, the biologically active form of vitamin B6, is a cofactor for over 140 biochemical reactions. Although severe vitamin B6 deficiency is...
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SubjectTerms	Animals Biomarkers - blood C-reactive protein C-Reactive Protein - metabolism chemical reactions chemotaxis Colitis Colon Colon - drug effects Colon - physiopathology Cyclooxygenase 2 - metabolism diet Dietary Supplements Disease Models, Animal Female genetic markers Helicobacter hepaticus Inflammation inflammatory bowel disease Inflammatory Bowel Diseases - drug therapy interferon-gamma Interferon-gamma - metabolism Interleukin-10 - metabolism interleukin-6 Interleukin-6 - metabolism Lysophospholipids - metabolism Male Mice Mice, Knockout Nitric Oxide Synthase Type II - metabolism pyridoxal Pyridoxal 5’ phosphate pyridoxine Shingosine 1 phosphate sphingosine Sphingosine - analogs & derivatives Sphingosine - metabolism tumor necrosis factor-alpha Tumor Necrosis Factor-alpha - metabolism United States Vitamin B 6 - administration & dosage Vitamin B 6 - blood weanlings
Title	Dietary vitamin B6 intake modulates colonic inflammation in the IL10−/− model of inflammatory bowel disease
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