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Biomedical subjects

R K Chandra

Publications and source records attributed to R K Chandra.

At least 109 records · Page 6Linked to original sources
PubMed1981

Serum thymic hormone activity and cell-mediated immunity in healthy neonates, preterm infants, and small-for-gestational age infants.

Groups of healthy, small-for-gestational age (SGA) and preterm appropriate-for-gestational age (AGA) infants were studied at birth, 1 month, 3 months, and 12 months of age. Serum thymic hormone (TH) activity was assayed, the number of T lymphocytes in the peripheral blood was counted, and in vitro lymphocyte stimulation responses to phytohemagglutinin (PHA) were evaluated. TH activity was decreased in 1-month-old SGA infants. T cells were reduced in all low birth weight infants; the number reverted to normal by 3 months of age in preterm AGA infants, whereas it remained low for at least 12 months in the SGA group. Lymphocyte stimulation response was decreased in low birth weight infants; the extent of depression paralleled reduction in T lymphocyte number. These observations indicate that cell-mediated immunity is impaired in low birth weight newborns and reduced TH activity may be one of the pathogenetic factors involved. Persistent depression of immunocompetence may underlie the increased susceptibility of SGA infants to infection-related morbidity and mortality.

Adult↗
PubMed1981

Immune response in overnutrition.

Nutritional modulation of the immune response can be demonstrated both in nutritional deficiency and in obesity. A proportion of obese adolescents and adults showed a variable impairment of cell-mediated immune responses in vivo and in vitro and reduction of intracellular bacterial killing by polymorphonuclear leukocytes. Immunological changes correlated with subclinical deficiencies of iron and zinc, and therapy with these micronutrients for 4 weeks resulted in improvement in immunological responses. In genetically obese mice, the number of mononuclear cells and Thy 1.2-positive lymphocytes in the thymus and the spleen is less compared with that in lean controls. The plaque-forming antibody response is reduced. Natural killer cell activity is increased. Cytotoxic response of spleen cells of obese animals immunized in vivo was markedly lower than that of lean controls, whereas the same response after in vitro sensitization was normal. These data point to the importance of metabolic and nutritional factors in the pathogenesis of altered immunocompetence.

Adolescent↗
PubMed1980

Cell-mediated immunity in genetically obese C57BL/6J ob/ob) mice.

The thymus and spleen of genetically obese (C57BL/6J ob/ob) mice weighed less and contained fewer mononuclear cells and Thy 1.2-positive lymphocytes compared with findings in lean controls. The number of splenic antibody forming cells, particularly IgG-producing lymphocytes, was reduced. There was a marked increase in natural killer cell activity and a slight increase in antibody-dependent cell-mediated cytotoxicity in the obese animals. Cytotoxic response of spleen cells of obese mice immunized in vivo was markedly lower than that of lean controls, whereas the generation of T killer cells against alloantigens after in vitro immunization was unimpaired, which points to a deleterious "microenvironment" in obesity. It is suggested that metabolic, nutritional, and endocrine changes in obesity may contribute to altered immunocompetence.

Animals↗
PubMed1980

Single nutrient deficiency and cell-mediated immune responses. I. Zinc.

The thymus of rats provided zinc-deficient diet weighed less than the thymus of animals fed zinc-containing control diet. The antibody-forming cell response in the spleen was reduced. Cytotoxic response of spleen cells of zinc-deficient mice immunized in vivo was decreased whereas after sensitization in vitro the response was comparable to that seen in zinc-replete animals. Natural killer cell activity and antibody-dependent cell-mediated cytotoxicity were increased, particularly the former. These observations suggest that dietary zinc intake is an important factor modulating cell-mediated immune responses.

Animals↗
PubMed1980

Effects of severe calorie restriction on thymic factor activity and lymphocyte stimulation response in rats.

The thymic factor (TF) activity and lymphocyte stimulation response to phytohemagglutinin (PHA) was studied in calorie-restricted rats. Sprague-Dawley rats (28 days old) were fed a calorie-restricted diet (30% of the average food intake of control) for 4 weeks. The control group was allowed food ad libitum. After this period the body weight was 232.9 +/- 41.8 g for control rats and 66.1 +/- 4.5 g for the calorie-restricted group. The mean thymus weight was 0.699 +/- 0.153 g and 0.099 +/- 0.030 g for the control and experimental groups respectively. The TF activity was makedly reduced in the calorie-restricted group compared with the control. There was an overlap between lymphocyte stimulation responses of the two groups; however, the mean number of counts per minute (cpm) of stimulated cultures with PHA was lower and the mean cpm of unstimulated cultures without PHA was higher in the starved animals. Thus, the stimulation index was significantly lower in the deprived rats. It is suggested that deficiency of thymic inductive factors may be important in the pathogenesis of impaired cell-mediated immunity in nutritional deficiency states.

Animals↗
PubMed1980

Immunocompetence in obesity.

Thirty-eight % of obese children and adolescents showed a variable impairment of cell-mediated immune responses in vivo and in vitro and reduction of intracellular bacterial killing by polymorphonuclear leukocytes. The obese group had a higher incidence of iron deficiency and moderately lower serum zinc concentrations. Levels of serum immunoglobulins, complement components C3 and C4, and numbers of T and B lymphocytes were comparable in the two groups. Serum triglycerides, cholesterol and lipoproteins were normal in all subjects. Immunologic changes correlated with the presence of subclinical deficiencies of iron and zinc. Therapy with these micronutrients for 4 weeks resulted in improvement in immunologic responses.

Adolescent↗
PubMed1980

Penicillin allergy: anti-penicillin IgE antibodies and immediate hypersensitivity skin reactions employing major and minor determinants of penicillin.

300 children considered to have had adverse reactions to penicillin were examined. Informed consent was obtained from the parents. Skin tests were conducted by the scratch/prick and intradermal techniques, using benzylpenicilloyl polylysine conjugate and a mixture of minor determinants of penicillin. Specific anti-penicillin IgE antibodies were estimated by the radioallergosorbent test. There was a good correlation between the two methods. The overall frequency of positive tests was 19%. 11 children showed cutaneous reactivity only to the minor determinants mixture. Positive results were found more often in those with accelerated adverse reactions, particularly anaphylaxis, serum sickness, angio-oedema, or urticaria. The validity of penicillin-negative results was confirmed by drug challenge in 56 subjects, only 2 of whom showed a slight skin rash. Of 5 patients with positive tests, inadvertent administration of penicillin produced accelerated urticaria in all. 14 of 42 children with positive tests had lost hypersensitivity to penicillin one year later. In a separate group of 50 children with a history of adverse response to ampicillin, the overall frequency of positive tests was 12%; 38% showed evidence of recent E-B virus infection. It was concluded that penicillin allergy is often overdiagnosed. The diagnosis can be reliably confirmed by skin tests using major and minor determinants of benzylpenicillin and by the radioallergosorbent test; such hypersensitivity is not permanent.

Ampicillin↗
PubMed1980

Spleen hemolytic plaque-forming cell response and generation of cytotoxic cells in genetically obese (C57Bl/6J ob/ob) mice.

Cell-mediated immune responses were evaluated in genetically obese (C57Bl/6J ob/ob) mice and lean controls. The thymus and spleen weighed less and contained fewer mononuclear cells in obese animals compared with controls. The total number of direct and indirect plaque-forming cells in the spleen of obese mice immunized intraperitoneally with sheep red blood cells was reduced, however, when the results were expressed as plaques/10(6) mononuclear cells, the proportion of antibody-producing cells was higher in the obese. Ob/ob mice immunized in vivo with allogeneic EL-4 lymphoma cells showed markedly diminished capacity to generate cytotoxic cells, whereas such response after in vitro immunization was comparable in the two groups of animals. These observations suggest that altered cell-mediated immune response in obese animals is the result of a deleterious microenvironment.

Animals↗
PubMed1980

Cell-mediated immunity in nutritional imbalance.

Marked perturbations of cell-mediated immunity are observed in nutritional imbalance, both undernutrition and overnutrition. Individuals with protein-energy malnutrition show consistent impairment of cutaneous delayed hypersensitivity and a reduced number of circulating T lymphocytes. Variable changes in lymphocyte stimulation response in vitro to mitogens and antigens are seen. There is a relative increase in the number of "null" cells and high levels of leukocyte terminal deoxynucleotidyl transferase activity. These findings suggest impaired differentiation of T cell precursors, which may be the direct result of reduced thymic hormone activity. Alterations in the production of lymphokines are not consistent. Infants with intrauterine growth retardation show a marked and long-lasting deficit in cell-mediated immunity. Specific nutrient deficiencies vary in their ability to influence cell-mediated immunity and the mechanisms underlying the immunologic abnormalities. Among others, zinc and pyridoxine deficiencies are associated with marked immunodepression. Obesity also is associated with alterations in cell-mediated immune responses. This has been observed in man, in genetically obese mice, and in states of excess intake of lipids, vitamins, minerals, and a trace elements. Nutritional modulation of cellular immunity is an important determinant of morbidity in several systemic disorders.

Autoimmune Diseases↗
PubMed1980

Serum thymic factor activity in deficiencies of calories, zinc, vitamin A and pyridoxine.

Cell-mediated immunity is invariably impaired in protein-energy malnutrition. The effect of selected nutrient deficiencies on serum thymic factor activity was assessed in deprived rats and pair-fed controls. Deficits of calories, zinc or pyridoxine resulted in significant lowering of serum thymic factor activity whereas vitamin A deficiency did not have any effect. It is suggested that variants nutrients modulate different steps of cell-mediated immunity and that reduced thymic hormone activity may be the underlying mechanism of imparied immunity in some but not all nutritional deficiencies.

Animals↗