Vitamin A supplementation leads to increases in regulatory CD4+Foxp3+LAP+ T cells in mice

Medeiros, Samara R.; Pinheiro-Rosa, Natália; Lemos, Luísa; Loli, Flavia G.; Pereira, Alline Gomes; Santiago, Andrezza Fernanda; Pinter, Ester C.; Alves, Andréa C.; Oliveira, Jamil S.; Cara, Denise Carmona; Maioli, Tatiani Uceli; Faria, Ana Maria Caetano

doi:10.1016/j.nut.2015.03.004

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…4 In mouse models, vitamin A deficiency leads to lower levels of CD4 1 Foxp3 1 inflammatory cytokines. 6 Vitamin A supplementation increased the frequencies of tissue Tregs in this animal model. In addition, T-cell homing to the intestine is regulated by vitamin A through regulation of intestinal homing molecules on the surface of the T cells, such as CCR9, modifying risk of gut inflammation.…”

Section: Introductionmentioning

confidence: 72%

“…We considered vitamin A as a candidate variable in this search because it modifies gut permeability in other clinical settings, is essential for development of mucosal tolerance, and regulates lymphocyte trafficking to the gut. [3][4][5][6][7][8][9][10][11][12] Vitamin A is an essential nutrient, ingested in the diet as preformed retinol. Levels in the blood are homeostatically regulated to maintain a narrow range, which is accomplished through cosecretion of retinol bound to its specific carrier protein, retinol-binding protein (RBP), from the liver.…”

Section: Introductionmentioning

confidence: 99%

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Lower levels of vitamin A are associated with increased gastrointestinal graft-versus-host disease in children

Lounder

Khandelwal

Dandoy

et al. 2017

Blood

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• Vitamin A levels below the median at day 30 posttransplant are associated with increased cumulative incidence of GI GVHD in children.• Potential mechanisms include increased intestinal permeability and increased lymphocyte homing to the intestine.Vitamin A promotes development of mucosal tolerance and enhances differentiation of regulatory T cells. Vitamin A deficiency impairs epithelial integrity, increasing intestinal permeability. We hypothesized that higher vitamin A levels would reduce the risk of graftversus-host disease (GVHD) through reduced gastrointestinal (GI) permeability, reduced mucosal injury, and reduced lymphocyte homing to the gut. We tested this hypothesis in a cohort study of 114 consecutive patients undergoing allogeneic stem cell transplant. Free vitamin A levels were measured in plasma at day 30 posttransplant. GI GVHD was increased in patients with vitamin A levels below the median (38% vs 12.4% at 100 days, P 5 .0008), as was treatment-related mortality (17.7% vs 7.4% at 1 year, P 5 .03). Bloodstream infections were increased in patients with vitamin A levels below the median (24% vs 8% at 1 year, P 5 .03), supporting our hypothesis of increased intestinal permeability. The GI mucosal intestinal fatty acid-binding protein was decreased after transplant, confirming mucosal injury, but was not correlated with vitamin A levels, indicating that vitamin A did not protect against mucosal injury. Expression of the gut homing receptor CCR9 on T-effector memory cells 30 days after transplant was increased in children with vitamin A levels below the median (r 5 20.34, P 5 .03). Taken together, these data support our hypothesis that low levels of vitamin A actively promote GI GVHD and are not simply a marker of poor nutritional status or a sicker patient. Vitamin A supplementation might improve transplant outcomes. (Blood. 2017;129(20):2801-2807

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Section: Introductionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Lower levels of vitamin A are associated with increased gastrointestinal graft-versus-host disease in children

Lounder

Khandelwal

Dandoy

et al. 2017

Blood

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“…Retinol metabolism is closely related to vitamin A (Ross and Zolfaghari 2004 ), which promotes the progression and function of the immune system (Medeiros et al. 2015 ). The model group in this study had high levels of retinoic acid rather than the control group, which was consistent with a study observed by Hu et al.…”

Section: Discussionmentioning

confidence: 99%

Metabolomics coupled with network pharmacology study on the protective effect of Keguan-1 granules in LPS-induced acute lung injury

Chen

Zhou

Zhao

et al. 2022

Pharmaceutical Biology

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Context Keguan-1 (KG-1) plays a vital role in enhancing the curative effects, improving quality of life, and reducing the development of acute lung injury (ALI). Objective To unravel the protective effect and underlying mechanism of KG-1 against ALI. Materials and methods C57BL/6J mice were intratracheally instilled with lipopolysaccharide to establish the ALI model. Then, mice in the KG-1 group received a dose of 5.04 g/kg for 12 h. The levels of proinflammatory cytokines, chemokines, and pathological characteristics were determined to explore the effects of KG-1. Next, untargeted metabolomics was used to identify the differential metabolites and involved pathways for KG-1 anti-ALI. Network pharmacology was carried out to predict the putative active components and drug targets of KG-1 anti-ALI. Results KG-1 significantly improved the levels of TNF-α (from 2295.92 ± 529.87 pg/mL to 1167.64 ± 318.91 pg/mL), IL-6 (from 4688.80 ± 481.68 pg/mL to 3604.43 ± 382.00 pg/mL), CXCL1 (from 4361.76 ± 505.73 pg/mL to 2981.04 ± 526.18 pg/mL), CXCL2 (from 5034.09 ± 809.28 pg/mL to 2980.30 ± 747.63 pg/mL), and impaired lung histological damage. Untargeted metabolomics revealed that KG-1 significantly regulated 12 different metabolites, which mainly related to lipid, amino acid, and vitamin metabolism. Network pharmacology showed that KG-1 exhibited anti-ALI effects through 17 potentially active components acting on seven putative drug targets to regulate four metabolites. Discussion and conclusions This work elucidated the therapeutic effect and underlying mechanism by which KG-1 protects against ALI from the view of the metabolome, thus providing a scientific basis for the usage of KG-1.

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“…RA may mitigate IBD severity through various immunoregulatory mechanisms. RA could: (1) restore and/or reprogram the impaired Treg/Th17 lineage differentiation that is usually linked to IBD development [ 51 , 107 ] by inducing adaptive Treg cells and imprinting their gut-homing phenotype in response to inflammatory stimuli [ 108 ]; (2) modulate the recognition of different TLR ligands and control the activation of downstream transcription factor signaling [ 109 , 110 ]; (3) downregulate inflammatory signaling molecules like nitric oxide (NO) from PBMCs of IBD patients, even after the establishment of the pro-inflammatory niche [ 111 ]; (4) regulate the production of immunoregulatory cytokines, such as by enhancing the synthesis of IL-22 by γδ T cells and ILCs and consequently attenuating colitis [ 61 ]; and (5) synergize with immunoregulatory mediators like TGFβ for maintaining gut homeostasis [ 112 ].…”

Section: Efficacies Of Ra In the Treatment Of Autoimmune Diseasesmentioning

confidence: 99%

Retinoic Acid, Leaky Gut, and Autoimmune Diseases

Abdelhamid

Luo

2018

Nutrients

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A leaky gut has been observed in a number of autoimmune diseases including type 1 diabetes, multiple sclerosis, inflammatory bowel disease, and systemic lupus erythematosus. Previous studies from our laboratory have shown that lupus mice also bear a leaky gut and that the intestinal barrier function can be enhanced by gut colonization of probiotics such as Lactobacillus spp. Retinoic acid (RA) can increase the relative abundance of Lactobacillus spp. in the gut. Interestingly, RA has also been shown to strengthen the barrier function of epithelial cells in vitro and in the absence of probiotic bacteria. These reports bring up an interesting question of whether RA exerts protective effects on the intestinal barrier directly or through regulating the microbiota colonization. In this review, we will discuss the roles of RA in immunomodulation, recent literature on the involvement of a leaky gut in different autoimmune diseases, and how RA shapes the outcomes of these diseases.

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Vitamin A supplementation leads to increases in regulatory CD4+Foxp3+LAP+ T cells in mice

Cited by 9 publications

References 17 publications

Lower levels of vitamin A are associated with increased gastrointestinal graft-versus-host disease in children

Lower levels of vitamin A are associated with increased gastrointestinal graft-versus-host disease in children

Metabolomics coupled with network pharmacology study on the protective effect of Keguan-1 granules in LPS-induced acute lung injury

Retinoic Acid, Leaky Gut, and Autoimmune Diseases

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