Folate Deficiency Inhibits the Proliferation of Primary Human CD8+ T Lymphocytes In Vitro

Courtemanche, Chantal; Elson-Schwab, Ilan; Mashiyama, Susan T.; Kerry, Nicole; Ames, Bruce N.

doi:10.4049/jimmunol.173.5.3186

Cited by 147 publications

(112 citation statements)

References 51 publications

(48 reference statements)

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“…There is some evidence that a deficiency or lack of folate intake significantly alters the immune response (Dhur et al, 1991;Courtemanche et al, 2004). Folate is related to lower concentrations of inflammatory markers and oxidative stress (Graham and O'Callaghan, 2000;Nanri et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Association of maternal folate nutrition and serum C-reactive protein concentrations with gestational age at delivery

Kim

Hwang

et al. 2010

Eur J Clin Nutr

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Background/objectives: C-reactive protein (CRP) is the most extensively studied inflammatory risk marker, and elevated serum CRP concentrations in pregnant women are known to be associated with subsequent development of preeclampsia and preterm delivery. Researchers have suggested that folate intake may help to control the inflammation process. We examined whether folate nutrition modifies the relationship between serum CRP concentration and gestational age at delivery. Subjects/methods: Serum CRP concentrations were analyzed in 815 pregnant women between 12 and 28 weeks of gestation. Dietary intakes were assessed using a 24-h dietary recall. The serum folate and high-sensitivity CRP concentrations were analyzed by radioassay and latex agglutination tests, respectively. Results: Serum CRP concentration was negatively correlated (Po0.001) with gestational age at delivery. Serum folate concentration was negatively correlated (Po0.01) with serum CRP concentration, and total dietary folate intake was positively correlated (Po0.001) with serum folate concentration. Multiple regression analysis after adjustment for covariates revealed that maternal CRP concentrations were negatively associated with gestational age at delivery; these negative associations existed only when folate intake during pregnancy was below the Korean estimated average requirements (520 mg dietary folate equivalent per day), and serum folate concentrations were above the normal (6 ng/ml). Conclusions: We found that adequate maternal folate intake during pregnancy may have a beneficial role against shorter gestational age at delivery, which is associated with higher serum CRP concentrations in pregnant women.

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Section: Introductionmentioning

confidence: 99%

Association of maternal folate nutrition and serum C-reactive protein concentrations with gestational age at delivery

Kim

Hwang

et al. 2010

Eur J Clin Nutr

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“…Large quantities of dUTP may be incorporated instead of dTTP during S-phase (or DNA repair). The resulting A:U mismatches, however, do not result in mutations, but may hamper recognition by DNA-binding proteins and thus alter physiological function (Courtemanche et al, 2004). Levels of uracil in the DNA of UngϪ/Ϫ cells strongly depend on proliferation (Andersen et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Folate Deficiency Induces Neurodegeneration and Brain Dysfunction in Mice Lacking Uracil DNA Glycosylase

Kronenberg

Harms²,

Sobol³

et al. 2008

J. Neurosci.

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Folate deficiency and resultant increased homocysteine levels have been linked experimentally and epidemiologically with neurodegenerative conditions like stroke and dementia. Moreover, folate deficiency has been implicated in the pathogenesis of psychiatric disorders, most notably depression. We hypothesized that the pathogenic mechanisms include uracil misincorporation and, therefore, analyzed the effects of folate deficiency in mice lacking uracil DNA glycosylase (UngϪ/Ϫ) versus wild-type controls. Folate depletion increased nuclear mutation rates in UngϪ/Ϫ embryonic fibroblasts, and conferred death of cultured UngϪ/Ϫ hippocampal neurons. Feeding animals a folate-deficient diet (FD) for 3 months induced degeneration of CA3 pyramidal neurons in UngϪ/Ϫ but not Ung؉/؉ mice along with decreased hippocampal expression of brain-derived neurotrophic factor protein and decreased brain levels of antioxidant glutathione. Furthermore, FD induced cognitive deficits and mood alterations such as anxious and despair-like behaviors that were aggravated in UngϪ/Ϫ mice. Independent of Ung genotype, FD increased plasma homocysteine levels, altered brain monoamine metabolism, and inhibited adult hippocampal neurogenesis. These results indicate that impaired uracil repair is involved in neurodegeneration and neuropsychiatric dysfunction induced by experimental folate deficiency.

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“…One in vitro study revealed that the proliferative activity of primary human CD8-positive cytotoxic T-lymphocytes was inhibited by folate deficiency [21]. It has also been demonstrated in vitro that folate deficiency induces apoptotic cell death of phytohemagglutinin-stimulated human primary lymphocytes from the blood through triggering mitochondrial membrane depolarization [22].…”

Section: Discussionmentioning

confidence: 99%

Folate-deficiency induced cell-specific changes in the distribution of lymphocytes and granulocytes in rats

Abe

Shirato

Hashizume

et al. 2012

Environ Health Prev Med

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Objective Folate (vitamin B 9 ) plays key roles in cell growth and proliferation through regulating the synthesis and stabilization of DNA and RNA, and its deficiency leads to lymphocytopenia and granulocytopenia. However, precisely how folate deficiency affects the distribution of a variety of white blood cell subsets, including the minor population of basophils, and the cell specificity of the effects remain unclear. Therefore, we examined the effects of a folate-deficient diet on the circulating number of lymphocyte subsets [T-lymphocytes, B-lymphocytes, and natural killer (NK) cells] and granulocyte subsets (neutrophils, eosinophils, and basophils) in rats. Methods Rats were divided into two groups, with one receiving the folate-deficient diet (FAD group) and the other a control diet (CON group). All rats were pair-fed for 8 weeks.Results Plasma folate level was dramatically lower in the FAD group than in the CON group, and the level of homocysteine in the plasma, a predictor of folate deficiency was significantly higher in the FAD group than in the CON group. The number of T-lymphocytes, B-lymphocytes, and NK cells was significantly lower in the FAD group than in the CON group by 0.73-, 0.49-, and 0.70-fold, respectively, indicating that B-lymphocytes are more sensitive to folate deficiency than the other lymphocyte subsets. As expected, the number of neutrophils and eosinophils was significantly lower in the FAD group than in the CON group. However, the number of basophils, the least common type of granulocyte, showed transiently an increasing tendency in the FAD group as compared with the CON group. Conclusion These results suggest that folate deficiency induces lymphocytopenia and granulocytopenia in a cellspecific manner.

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Folate Deficiency Inhibits the Proliferation of Primary Human CD8+ T Lymphocytes In Vitro

Cited by 147 publications

References 51 publications

Association of maternal folate nutrition and serum C-reactive protein concentrations with gestational age at delivery

Association of maternal folate nutrition and serum C-reactive protein concentrations with gestational age at delivery

Folate Deficiency Induces Neurodegeneration and Brain Dysfunction in Mice Lacking Uracil DNA Glycosylase

Folate-deficiency induced cell-specific changes in the distribution of lymphocytes and granulocytes in rats

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