1,25-Dihydroxyvitamin D3 and the regulation of macrophage function

Bar‐Shavit, Zvi; Noff, Dina; Edelstein, S.; Meyer, Manuela; Shibolet, Shlomo; Goldman, Rachel

doi:10.1007/bf02409507

Cited by 140 publications

(47 citation statements)

References 15 publications

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“…Analysis of the immune system of the vitamin Ddeficient mice at 100 days of age, time when animals were switched to normal food, showed major abnormalities in macrophage behaviour. The differences were, however, not situated in impaired phagocytosis or chemotaxis, previously observed in severe rickets [7,25,26,27]. The near normal phagocytic and chemotactic capacity confirms again the relevance of our model, where we did not create severely rachitic mice, but only induced a vitamin deficiency frequently observed in children.…”

Section: Discussionsupporting

confidence: 76%

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

et al. 2004

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Aims/hypothesis. 1,25-dihydroxyvitamin D 3 , the active form of vitamin D, prevents Type 1 diabetes in non-obese diabetic (NOD) mice. Epidemiological data show a threefold increase in human Type 1 diabetes when vitamin D deficiency was present in the first months of life. To evaluate whether a similar dietary deficiency affects diabetes incidence in NOD mice, we generated NOD mice with vitamin D deficiency in early life. Methods. Breeding pairs of NOD mice, as well as their offspring (test mice), were kept in surroundings devoid of ultraviolet light and were fed a vitamin Ddepleted diet for 100 days. Mice were followed for 250 days. Results. At 250 days, 35% (12/35) male and 66% (22/33) female vitamin D-deficient mice were diabetic compared to 15% (6/40, p=0.05) and 45% (13/29, p<0.01) of the control mice. At 100 days no difference in insulitis was seen, but more vitamin D-deficient mice were glucose intolerant. Higher IL1 expression was detected in islets of vitamin D-deficient mice and their peritoneal macrophages had an aberrant cytokine profile (low IL1 and IL6, high IL15). Thymus and lymph nodes of vitamin D-deficient mice contained less CD4 + CD62L + cells. Conclusion/interpretation. Vitamin D status increases the expression of Type 1 diabetes in NOD mice. Our data in NOD mice, as well as human epidemiological data, point to the importance of preventing vitamin D deficiency in early childhood. Controlling this dietary factor could be an easy and safe way to reduce the incidence of Type 1 diabetes in subjects who are genetically at risk. [Diabetologia (2004)

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Section: Discussionsupporting

confidence: 76%

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

et al. 2004

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“…Since vitamin D 3 increases phagocytosis via the activation of macrophages and affects immune response, it is potentially involved in the development of several diseases (8). Vitamin D 3 may limit the growth of M. tuberculosis in macrophages (7).…”

Section: Introductionmentioning

confidence: 99%

Association between vitamin D receptor polymorphisms and haplotypes with pulmonary tuberculosis

et al. 2014

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Abstract. The vitamin D receptor (VDR) is an important factor in activating immune response in different infectious diseases. The aim of the present study was to investigate the association between the VDR gene polymorphisms and pulmonary tuberculosis (PTB). The case control study was performed on 120 PTB patients and 131 healthy controls. Genetic analysis was performed by polymerase chain reaction and the restriction fragment length polymorphism method. The VDR Fok1 Ff genotype was associated with TB and the risk of PTB was two times higher in individuals with the Ff genotype. A higher frequency of f allele was observed in PTB patients and therefore, the f allele may be a risk factor for PTB susceptibility. There were no associations between the Taq1 and Bsm1 polymorphisms and PTB. In addition, haplotype analysis showed that the f-T-B and f-t-b haplotypes (Fok1, Taq1 and Bsm1) may have the potential to increase PTB susceptibility. In conclusion, the Ff genotype and f allele of the VDR Fok1 polymorphism were associated with PTB susceptibility. In addition, the f-T-B and f-t-b haplotypes may be the susceptible haplotypes for PTB. IntroductionTuberculosis (TB) is the result of infection with Mycobacterium tuberculosis (M. tuberculosis) and is a significant cause of morbidity and mortality worldwide. Each year >9 million people are infected by TB and >1.7 million succumb to TB annually (1). The incidence of TB in Iran has been reported as 13.7 per 100,000 in 2009; however, its incidence was higher in the Sistan-Balouchestan province, southeastern Iran. The higher incidence is due to bordering with Afghanistan and Pakistan; two countries with a high TB prevalence (2). Cell-mediated immunity is essential for suppression of Mycobacterial infection as it is an intracellular parasite (3). The fact that only 10% of those infected with M. tuberculosis progress to clinical disease revealed that genetic factors, as well as environmental factors are involved in the pathophysiology of TB (4).In addition, the host genetic basis of TB has been confirmed by twin studies that indicated a two times higher risk of disease in identical twins compared to non-identical twins (5).Several genes have been found to play a role in TB susceptibility and the relative significance of these genes in disease progression or various forms of disease is often modified by the ethnicity in different populations (6).The active form of vitamin D, 1-25-dihydroxyvitamin D 3 , is an important hormone that modulates the activity of different defense and immune cells, including lymphocytes, monocytes, macrophages and epithelial cells (7). Since vitamin D 3 increases phagocytosis via the activation of macrophages and affects immune response, it is potentially involved in the development of several diseases (8). Vitamin D 3 may limit the growth of M. tuberculosis in macrophages (7). Vitamin D 3 exerts its effects through the vitamin D receptor (VDR) and regulates numerous target genes by binding to its nuclear receptor. Active VDR binds to vitamin D response...

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“…Children with vitamin D deficiency appear to have a high incidence of infection [26], and vitamin D-deficient rat macrophages showed abnormalities in phagocytic and microbicidal activities [27], suggesting that vitamin D is one of the important factors for defense against microbial infection. However, our patients with VDDR II did not show any recurrent infection throughout their lives, and MDM from these patients normally responded to 1,25(OH)2D3.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D₃ elicits calcium response and activates blood monocyte‐derived macrophages from patients with vitamin D dependent rickets type II

et al. 1996

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We preferentially used MDM from peripheral blood in this study, since 1,25(OH)2D3 is one of the inducers of differentiation of a monocyte-macrophage lineage and is also a potent activator for macrophage functions. The activation of macrophages by 1,25(OH)2D3 results in enhanced capacity for production of microbicidal oxygen metabolites [8,9]. In this paper, we studied the effects of 1,25(OH)gD3 on calcium response and superoxide anion (O~-) release in MDM from patients with VDDR II to assess the role of VDR in macrophage functions.

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1,25-Dihydroxyvitamin D3 and the regulation of macrophage function

Cited by 140 publications

References 15 publications

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

Association between vitamin D receptor polymorphisms and haplotypes with pulmonary tuberculosis

Vitamin D₃ elicits calcium response and activates blood monocyte‐derived macrophages from patients with vitamin D dependent rickets type II

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1,25-Dihydroxyvitamin D3 and the regulation of macrophage function

Cited by 140 publications

References 15 publications

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

Vitamin D deficiency in early life accelerates Type 1 diabetes in non-obese diabetic mice

Association between vitamin D receptor polymorphisms and haplotypes with pulmonary tuberculosis

Vitamin D3 elicits calcium response and activates blood monocyte‐derived macrophages from patients with vitamin D dependent rickets type II

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Vitamin D₃ elicits calcium response and activates blood monocyte‐derived macrophages from patients with vitamin D dependent rickets type II