Vitamin A Deficiency Impairs Induction of Oral Tolerance in Mice

Nakamoto, Akiko; Shuto, Emi; Tsutsumi, Rie; Nakamoto, Mariko; Nii, Yoshitaka; Sakai, Tohru

doi:10.3177/jnsv.61.147

Cited by 11 publications

(10 citation statements)

References 36 publications

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“…In neonate mice vitamin A deficiency (VAD) resulted in impairment of oral tolerance induction [ 24 ] with insufficient Treg cell activation by DCs in mesenteric lymph nodes as possible underlying mechanism [ 25 ]. Interestingly, feeding of a single dose of vitamin A in adult mice could amplify the tolerogenic properties of mesenteric lymph node DCs [ 26 ].…”

Section: Correlation Of Vitamin A/d Deficiency With Allergic Immune Rmentioning

confidence: 99%

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Hufnagl

Jensen‐Jarolim

2018

Allergo J Int

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IntroductionVitamins A and D are able to modulate innate and adaptive immune responses and may therefore influence the development and the course of allergic diseases.Materials and methodsThis article reviews the current evidence for the experimental effects of vitamins A and D in vivo in animal models and on immune cells in vitro, and discusses their translational implication. A systematic literature search over the last 10 years was performed using MEDLINE and PubMed databases.ResultsDeficiencies of vitamin A or vitamin D in mouse models of allergic asthma seem to exacerbate allergic symptoms along with enhanced lung inflammation and Th2 cytokine production. In contrast, supplementation regimes especially with vitamin D were able to attenuate symptoms in therapeutic mouse models. The active metabolites retinoic acid (RA) and 1,25-dihydroxyvitamin D3 (VD3) induced tolerogenic dendritic cells (DCs) and up-regulated T‑regulatory cells in the allergic sensitization phase, which likely contributes to tolerance induction. Additionally, RA and VD3 maintained the stability of eosinophils and mast cells in the effector phase, thereby reducing allergic mediator release. Thus, both active vitamin metabolites RA and VD3 are able to influence allergic immune responses at several immunological sites.ConclusionAnimal studies predict that vitamin A and D may also be attractive players in the control of allergy in humans. Whether these experimental observations can be translated to the human situation remains open, as results from clinical trials are controversial.

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Section: Correlation Of Vitamin A/d Deficiency With Allergic Immune Rmentioning

confidence: 99%

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Hufnagl

Jensen‐Jarolim

2018

Allergo J Int

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“…Intestinal studies in vivo and vitro showed that sufficient retinoic acid (a kind of metabolites of vitamin A) can promote intestinal regulatory T cells productions 39,40 . Akiko et al 41 stated the differentiation of Foxp3 + Treg from naïve CD4 + T cell is decreased in vitamin A deficient mice. Animal studies suggest that sufficient vitamin A can suppress Th2 reaction and promote Foxp3 + Treg and Th1 cells productions [42][43][44] .…”

Section: Discussionmentioning

confidence: 99%

Vitamin A supplement after neonatal Streptococcus pneumoniae pneumonia inhibits the progression of experimental asthma by altering CD4+T cell subsets

Tian

et al. 2020

Sci Rep

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Studies demonstrated that pneumonia can decrease vitamin A productions and vitamin A reduction/ deficiency may promote asthma development. Our previous study showed that neonatal Streptococcus pneumoniae (S. pneumoniae) infection promoted asthma development. Whether neonatal S. pneumoniae pneumonia induced asthma was associated with vitamin A levels remains unclear. The aim of this study was to investigate the effects of neonatal S. pneumoniae pneumonia on vitamin A expressions, to explore the effects of vitamin A supplement after neonatal S. pneumoniae pneumonia on adulthood asthma development. Non-lethal S. pneumoniae pneumonia was established by intranasal inoculation of neonatal (1-week-old) female BALB/c mice with D39. S. pneumoniae pneumonia mice were supplemented with or without all-trans retinoic acid 24 hours after infection. Vitamin A concentrations in lung, serum and liver were measured post pneumonia until early adulthood. Four weeks after pneumonia, mice were sensitized and challenged with OVA to induce allergic airway disease (AAD). Twenty-four hours after the final challenge, the lungs and bronchoalveolar lavage fluid (BALF) were collected to assess AAD. We stated that serum vitamin A levels in neonatal S. pneumoniae pneumonia mice were lower than 0.7µmol/L from day 2-7 post infection, while pulmonary vitamin A productions were significantly lower than those in the control mice from day 7-28 post infection. Vitamin A supplement after neonatal S. pneumoniae pneumonia significantly promoted Foxp3 + treg and Th1 productions, decreased Th2 and Th17 cells expressions, alleviated airway hyperresponsiveness (AHR) and inflammatory cells infiltration during AAD. Our data suggest that neonatal S. pneumoniae pneumonia induce serum vitamin A deficiency and long-time lung vitamin A reduction, vitamin A supplement after neonatal S. pneumoniae pneumonia inhibit the progression of asthma by altering CD4 + T cell subsets. Asthma is a heterogeneous disease characterized by airway chronic inflammation together with airway hyperresponsiveness 1. Asthma is more common in childhood, and most adult asthma originate from childhood, which suggesting childhood events play an important role in the pathogenesis of asthma 2-4. Childhood is a pivotal period for the immune system maturation. Specific pathogen may play a critical role in the allergic airway diseases (AAD) pathogenesis by affecting the immune system 5. Epidemiological studies show that neonates colonized with S. pneumoniae, Haemophilus influenzae or Moraxella catarrhalis significantly increases the risk of asthma in the first 5 years of life 6,7. S. pneumoniae is the most common bacterial pathogen of community acquired pneumonia in childhood. Our previous study suggested that neonatal S. pneumoniae infection promoted OVA-induced

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“…Intestinal studies in vivo and in vitro showed that sufficient retinoic acid (A kind of metabolites of vitamin A) can promote regulatory T cells productions [44, 45] . Akiko et al [46] stated the differentiation of Foxp3 + Treg from naïve CD4 + T cell is decreased in vitamin A deficient mice. Animal studies suggest that sufficient vitamin A can suppress Th2 reaction and promote Foxp3 + Treg and Th1 cells productions [47–49] .…”

Section: Discussionmentioning

confidence: 99%

Vitamin A supplement after neonatalStreptococcus pneumoniaepneumonia alters CD4⁺T cell subset and inhibits allergic asthma in mice model

Tian

et al. 2018

Preprint

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16 Background : Previously, we showed that neonatal pneumonia caused by Streptococcus 17 pneumoniae (S. pneumoniae) promoted adulthood ovalbumin (OVA) induced allergic 18 asthma. Many studies have demonstrated that vitamin A deficiency induced the development of 19 allergic asthma. Whether neonatal S. pneumoniae pneumonia promoted allergic asthma 20 development was associated with vitamin A concentrations remains unclear. 21 Methods: Female BALB/c neonates were infected with S. pneumoniae strain D39 and 22 subsequently treated with vitamin A. Vitamin A concentrations in lung, serum and liver were 23 monitored on 2, 5, 7, 14, 21, 28 days post infection. Four weeks after infection, mice were 24 sensitized and challenged with OVA to induce allergic airway disease (AAD) in early adulthood. 25 Twenty-four hours after the final challenge, lung histo-pathology, cytokine concentrations in 26 bronchoalveolar lavage fluid (BALF), airway hyperresponsiveness (AHR) and lung CD4 + T cells 27 were measured. 28 Results: We demonstrated that neonatal S. pneumoniae pneumonia induce lung vitamin A 29 deficiency up to early adulthood. Moreover, neonatal S. pneumoniae pneumonia aggravated 30 airway inflammatory cells accumulation and increased AHR during AAD, decreased Foxp3 + Treg 31 and Th1 productions remarkably, while Th2 cell expression was increased significantly. Further 32 study indicated that vitamin A supplement after neonatal S. pneumoniae pneumonia can promote 33 Foxp3 + Treg and Th1 productions, decrease Th2 cell expressions, alleviate AHR and inflammatory 34 cells infiltration during AAD. 35 Conclusions: Using a mouse model, we demonstrate that Vitamin A supplement after neonatal 36

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Vitamin A Deficiency Impairs Induction of Oral Tolerance in Mice

Cited by 11 publications

References 36 publications

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Vitamin A supplement after neonatal Streptococcus pneumoniae pneumonia inhibits the progression of experimental asthma by altering CD4+T cell subsets

Vitamin A supplement after neonatalStreptococcus pneumoniaepneumonia alters CD4⁺T cell subset and inhibits allergic asthma in mice model

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Vitamin A Deficiency Impairs Induction of Oral Tolerance in Mice

Cited by 11 publications

References 36 publications

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Vitamin A supplement after neonatal Streptococcus pneumoniae pneumonia inhibits the progression of experimental asthma by altering CD4+T cell subsets

Vitamin A supplement after neonatalStreptococcus pneumoniaepneumonia alters CD4+T cell subset and inhibits allergic asthma in mice model

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Vitamin A supplement after neonatalStreptococcus pneumoniaepneumonia alters CD4⁺T cell subset and inhibits allergic asthma in mice model