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Gāndhī Nagar, India

Vijayendra Chary A.,National Institute of Nutrition NIN | Hemalatha R.,National Institute of Nutrition NIN | Seshacharyulu M.,National Institute of Nutrition NIN | Vasudeva Murali M.,Gandhi Hospital | And 2 more authors.
Journal of Steroid Biochemistry and Molecular Biology | Year: 2015

Regulatory T cells and IgE receptors (CD23 and CD21) on B cells were assessed in vitamin D deficient pregnant women. For this, 153 pregnant women were recruited from a government hospital and were categorized into three groups based on 25-hydroxyvitamin D3 (25(OH)D3) status. Regulatory T cell population (Treg cells) and CD23/CD21 expression on B cells were quantified by FACS ARIA II in maternal blood at third trimester; and the same parameters were evaluated in cord blood soon after delivery. In addition, TGF β and IL-10 were quantified in maternal and cord blood by using Milliplex kits. In a representative sample of eight women from each group (vitamin D sufficient, insufficient and deficient), placental tissues were processed for mRNA expressions of vitamin D receptor (VDR), retinoic acid receptor (RXR), vitamin D binding protein (VDBP) and vitamin D regulating enzymes. Of the 153 pregnant women, 18 were sufficient (≥30 ng/mL), 55 were insufficient (20-29 ng/mL) and 80 were deficient (≤19 ng/mL) for 25(OH)D3 status. The maternal blood Treg cell population (mean (%) plusmn SE) was lower (p ;lt 0.05) in 25(OH)D3 deficient (0.2 plusmn 0.01) pregnant women compared to insufficient (0.34 ± 0.01) and sufficient (0.45 ± 0.02) pregnant women. Similarly, cord blood Treg cell population (mean (%) ± SE) was also lower (p < 0.05) in 25(OH)D3 deficient (0.63 ± 0.03) pregnant women when compared to insufficient (1.05 ± 0.04) and sufficient (1.75 ± 0.02) pregnant women. Mean (%) ± SE of B cells with CD23 and CD21 in maternal blood was higher (p < 0.05) in 25(OH)D3 deficient pregnant women (0.35 ± 0.02; 1.65 ± 0.04) when compared to insufficient (0.22 ± 0.02; 0.55 ± 0.05) and sufficient (0.15 ± 0.02; 0.21 ± 0.01) pregnant women. Similarly, mean (%) ± SE of B cell population with CD23 and CD21 in cord blood was also higher (p < 0.05) in 25(OH)D3 deficient (0.41 ± 0.02; 1.2 ± 0.03) when compared to insufficient (0.32 ± 0.01; 0.6 ± 0.05) and sufficient (0.2 ± 0.01; 0.4 ± 0.02) pregnant women. Regulatory cytokines, TGF β and IL-10 were lower (p < 0.05) in 25(OH)D3 insufficient and deficient subjects. In the placenta tissue of women with 25(OH)D3 deficiency, the regulatory T cell transcription factor FOXP3, vitamin D receptor (VDR) and retinoic acid receptor (RXR) expressions were downregulated. In contrast, CD23, CD21 and VDBP expressions were upregulated in 25(OH)D3 deficient and insufficient women. Vitamin D regulating enzymes (CYP24A1, CYP2R1 and CYP27B1) expression were also altered in women with 25(OH)D3 deficiency. The current study shows that impaired maternal 25(OH)D3 during pregnancy influences the spectrum of immune cells such as regulatory T cells and B cells with IgE receptors and this in turn may be linked to allergy and asthma in neonates. ©2014 Elsevier Ltd.


Vijayendra Chary A.,National Institute of Nutrition NIN | Hemalatha R.,National Institute of Nutrition NIN | Seshacharyulu M.,National Institute of Nutrition NIN | Vasudeva Murali M.,Gandhi Hospital | And 2 more authors.
Journal of Steroid Biochemistry and Molecular Biology | Year: 2015

Regulatory T cells and IgE receptors (CD23 and CD21) on B cells were assessed in vitamin D deficient pregnant women. For this, 153 pregnant women were recruited from a government hospital and were categorized into three groups based on 25-hydroxyvitamin D3 (25(OH)D3) status. Regulatory T cell population (Treg cells) and CD23/CD21 expression on B cells were quantified by FACS ARIA II in maternal blood at third trimester; and the same parameters were evaluated in cord blood soon after delivery. In addition, TGF β and IL-10 were quantified in maternal and cord blood by using Milliplex kits. In a representative sample of eight women from each group (vitamin D sufficient, insufficient and deficient), placental tissues were processed for mRNA expressions of vitamin D receptor (VDR), retinoic acid receptor (RXR), vitamin D binding protein (VDBP) and vitamin D regulating enzymes. Of the 153 pregnant women, 18 were sufficient (≥30 ng/mL), 55 were insufficient (20-29 ng/mL) and 80 were deficient (≤19 ng/mL) for 25(OH)D3 status. The maternal blood Treg cell population (mean (%) ± SE) was lower (p < 0.05) in 25(OH)D3 deficient (0.2 ± 0.01) pregnant women compared to insufficient (0.34 ± 0.01) and sufficient (0.45 ± 0.02) pregnant women. Similarly, cord blood Treg cell population (mean (%) ± SE) was also lower (p < 0.05) in 25(OH)D3 deficient (0.63 ± 0.03) pregnant women when compared to insufficient (1.05 ± 0.04) and sufficient (1.75 ± 0.02) pregnant women. Mean (%) ± SE of B cells with CD23 and CD21 in maternal blood was higher (p < 0.05) in 25(OH)D3 deficient pregnant women (0.35 ± 0.02; 1.65 ± 0.04) when compared to insufficient (0.22 ± 0.02; 0.55 ± 0.05) and sufficient (0.15 ± 0.02; 0.21 ± 0.01) pregnant women. Similarly, mean (%) ± SE of B cell population with CD23 and CD21 in cord blood was also higher (p < 0.05) in 25(OH)D3 deficient (0.41 ± 0.02; 1.2 ± 0.03) when compared to insufficient (0.32 ± 0.01; 0.6 ± 0.05) and sufficient (0.2 ± 0.01; 0.4 ± 0.02) pregnant women. Regulatory cytokines, TGF β and IL-10 were lower (p < 0.05) in 25(OH)D3 insufficient and deficient subjects. In the placenta tissue of women with 25(OH)D3 deficiency, the regulatory T cell transcription factor FOXP3, vitamin D receptor (VDR) and retinoic acid receptor (RXR) expressions were downregulated. In contrast, CD23, CD21 and VDBP expressions were upregulated in 25(OH)D3 deficient and insufficient women. Vitamin D regulating enzymes (CYP24A1, CYP2R1 and CYP27B1) expression were also altered in women with 25(OH)D3 deficiency. The current study shows that impaired maternal 25(OH)D3 during pregnancy influences the spectrum of immune cells such as regulatory T cells and B cells with IgE receptors and this in turn may be linked to allergy and asthma in neonates. © 2015 Elsevier Ltd. All rights reserved.


Chary A.V.,National Institute of Nutrition | Hemalatha R.,National Institute of Nutrition | Murali M.V.,Gandhi Hospital | Jayaprakash D.,Osmania University | Kumar B.D.,National Institute of Nutrition
Annals of Allergy, Asthma and Immunology | Year: 2016

Background Children with asthma have low vitamin D levels; however, we do not know whether low vitamin D is associated with impaired T-regulatory (Treg) cell population or high IgE receptors (CD23 and CD21) on B cells. Objective To examine Treg cell function, CD23 and CD21 receptors, vitamin D, and vitamin D-regulating enzymes in children with asthma. Methods Sixty children (2-6 years old) with asthma and 60 age-matched healthy children were selected as study participants. After collecting demographic and clinical data, blood samples were collected. Treg cells and CD23/CD21 expressions were evaluated by flow cytometry, 25-hydroxyvitamin D3 (25[OH]D3) was quantified by high-performance liquid chromatography, and cytokines and total IgE were estimated by enzyme-linked immunosorbent assay. Messenger RNA (mRNA) expressions of FOXP3, CD23, CD21, vitamin D receptors, and vitamin D-regulating enzymes were assessed by reverse transcription-polymerase chain reaction. Results The 25(OH)D3 concentrations and proportion of Treg cells were lower (P <.05) among children with asthma. In contrast, the proportions of B cells with CD23 and CD21 expression were higher (P <.05) in patients with asthma compared with controls. Interleukin 10 and transforming growth factor β were also altered in asthma. The mRNA expression of CD23, CD21, and vitamin D receptors was up-regulated, whereas mRNA expression of vitamin D-regulating enzymes, CYP2R1, CYP27B1, and vitamin D binding protein (except CYP24A1) were up-regulated among children with asthma. Conclusion The current study found impaired Treg cell population and high numbers of B cells with IgE receptors (CD23 and CD21) and altered regulatory cytokines in children with asthma, suggesting impaired immune regulation. © 2016 American College of Allergy, Asthma & Immunology.


Kavutharapu S.,Osmania University | Nagalla B.,National Institute of Nutrition | Abbagani V.,Gandhi Hospital | Porika S.K.,Osmania University | And 3 more authors.
Saudi Journal of Gastroenterology | Year: 2012

Background/Aim: Chronic pancreatitis (CP) is the progressive and irreversible destruction of the pancreas characterized by the permanent loss of endocrine and exocrine function. Trypsin, the most important digestive enzyme plays a central role in the regulation of all other digestive enzymes. Chymotrypsin, an endopeptidase hydrolyzes peptides at amino acids with aromatic side chains. Alpha-1-antitrypsin is a principal antiprotease which protects the mucosal tissue from the proteolytic effects of trypsin and chymotrypsin by the formation of molar complexes. The present study is aimed at examining the role of proteases (trypsin and chymotrypsin) and anti-protease (1-anti-trypsin) in the etiopathogenesis of chronic pancreatitis. Patients and Methods: A total of 90 CP patients and 110 age and sex matched controls were considered for the study. Serum trypsin, chymotrypsin and 1-anti-trypsin levels were determined prospectively in CP patients and compared to healthy controls as described previously. Results: The mean activity of trypsin were found to be increased in CP patients (X SD = 0.82 0.838) in comparison to normal control group (X SD = 0.55 0.328), (P = 0.001). Chymotrypsin activity were also found to be elevated in CP patients (X SD = 0.63 0.278) in comparison to control group (X SD = 0.39 0.295), (P = 0.0001). The mean -1-anti-trypsin activity were found to be lowered in CP patients (X SD = 0.42 0.494) in comparison to control group (X SD = 0.67 0.465), with the variation being significant (P = 0.0003). Conclusion: The findings suggest an imbalance in the synthesis and degradation of proteolytic enzymes and antiprotease indicating an altered aggressive and defensive role in the pathogenesis of chronic pancreatitis.


Ravi Kanth V.V.,Osmania University | Golla J.P.,Osmania University | Golla J.P.,U.S. National Institutes of Health | Sastry B.K.S.,Care Hospital | And 3 more authors.
Journal of Cardiovascular Disease Research | Year: 2011

Background: Researchers have determined that Indians face a higher risk of heart disease, despite the fact that nearly half of them are vegetarians and lack many of the other traditional risk factors. In the below-30 age group, coronary artery disease mortality among Indians is three-fold higher than in the whites in United Kingdom and ten-fold higher than the Chinese in Singapore. High levels of homocysteine have been widely linked to the early onset of heart diseases in other populations, although a definite proof among Indians is lacking, which needs to be investigated by way of screening for factors responsible for high homocysteine levels. Objective: To screen for genetic factors responsible for hyperhomocysteinemia and the risk for premature coronary artery disease. Materials and Methods: A total of 100 individuals with proven premature coronary artery disease and 200 age-and-sex matched controls were screened for polymorphisms in Methylenetetrahydrofolate reductase (MTHFR) (C677T) Methionine synthase (MS) genes (A2756G, C2758G), and the B12 and Folate levels were estimated. Results: Results from the mutational analysis revealed that in the study group, seven individuals had a polymorphism for the C677T allele in the MTHFR gene (one homozygous and six heterozygous) (Fischer′s Exact test P > 0.046) (OR: 0.2711 95% CI 0.0774 to 0.9491). Six were heterozygous for the A2756G polymorphism in the MS gene (Fischer′s Exact test P > 0.0012). None showed a polymorphism at the C2758G allele in the MS gene. Four controls showed heterozygosity for the C677T polymorphism and none for the MS gene. The B12 and Folate levels were significantly lower in the study group as compared to the controls. Conclusions: It is important to know which factors determine the total homocysteine concentrations. In the general population, the most important modifiable determinants of tHcy are folate intake and coffee consumption. Smoking and alcohol consumption are also associated with the total homocysteine concentrations, but more research is necessary to elucidate whether these relations are not originating from residual confounding due to other lifestyle factors.

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