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Biomedical subjects

R K Chandra

Publications and source records attributed to R K Chandra.

At least 91 records · Page 5Linked to original sources
PubMed1985

Nutritional regulation of host resistance and predictive value of immunologic tests in assessment of outcome.

In this review, the authors describe the current information on nutrition modulation of immunity, enumerate the various immunologic tests that are potentially useful in nutritional assessment, examine the reliability of tests predicting disease and complications, and discuss how immunologic evaluation may help in the decision process regarding nutritional support.

Antigen-Antibody Complex↗
PubMed1985

Grace A. Goldsmith Award lecture. Trace element regulation of immunity and infection.

Protein-calorie malnutrition is associated with impaired immunocompetence and increased susceptibility to infection. Clinically evident nutritional deficiency syndromes, however, are composite of deficits of many essential nutrients, each of which may exert an important regulating effect on immunity. Among other nutrients, several trace elements have been shown to regulate immune responses, particularly cell-mediated immunity. Zinc undernutrition results in lymphoid atrophy and reduced capacity to respond to many T-cell-dependent antigens. Plaque forming cell response to heterologous erythrocytes is decreased, as is the function of B cells. In zinc deficient rodents, the generation of cytotoxic lymphocytes in the spleen is reduced. Antibody-dependent cell-mediated cytotoxicity is largely unchanged. In acrodermatitis enteropathica, lymphocyte proliferation response to mitogens is decreased and there are significant changes in delayed hypersensitivity responses and in the proportion of various T cell subsets. Neutrophil function is not changed by zinc deficiency. Iron deficiency results in a slight decrease in the number of rosette-forming T cells and a significant impairment of lymphocyte response to mitogens and antigens. Polymorphonuclear leukocytes are unable to kill ingested bacteria and fungi in an efficient manner. Copper deficiency impairs cell-mediated immunity, as does selenium deficiency when it is associated with vitamin E lack. Several pathogenetic mechanisms may underlie such alterations in immunity. Many heavy metals impair immune responses. These effects of trace elements on immunity may have important fundamental and practical implications.

Animals↗
PubMed1985

Predictive value of cord blood IgE in the development of atopic disease and role of breast-feeding in its prevention.

The predictive value of cord blood IgE in the development of atopic disease was evaluated in a prospective study of two groups of infants. Total serum IgE level was greater than or equal to 0.7 U/ml in 44.3% of the infants with positive family history of atopy and in 16.0% among those with negative family history. The level of cord blood IgE correlated significantly with the subsequent development of atopic disease in both groups. Cord blood IgE higher than 0.7 U/ml was associated with a high risk of development of atopic eczema and wheezing, 52.8% and 58.8% respectively in the groups with or without family history of atopy; compared with 13.4% and 1.1% in the groups with IgE levels less than 0.7 U/ml. Among newborns fed exclusively on breast milk for a minimum of 3 months, the incidence of eczema and wheezing was significantly lower (12%) compared with findings in the formula-fed group (32%).

Breast Feeding↗
PubMed1984

Excessive intake of zinc impairs immune responses.

The effect of administration of large amounts of zinc on immune response and serum lipoproteins was examined. Eleven healthy adult men ingested 150 mg of elemental zinc twice a day for six weeks. This was associated with a reduction in lymphocyte stimulation response to phytohemagglutinin as well as chemotaxis and phagocytosis of bacteria by polymorphonuclear leukocytes. Serum high-density lipoprotein concentration decreased significantly and low-density lipoprotein level increased slightly. The common food fad of zinc supplementation with resultant excessive intake could have deleterious effects in healthy persons.

Adult↗
PubMed1984

Antibody affinity and immune complexes after immunization with tetanus toxoid in protein-energy malnutrition.

Protein-energy malnutrition reduced the affinity of antibody to tetanus toxoid, particularly after primary immunization. The effect on antibody affinity was more marked in patients with hypoproteinemia than in those with marasmus. Hemagglutinating antibody levels were comparable in undernourished and well-nourished groups. Circulating immune complexes were detected in eight of 21 children with protein-energy malnutrition and in one of the controls. Differences in antibody affinity in malnutrition may be an important determinant of altered host resistance and of complications of disease in nutritional deficiency.

Antibody Affinity↗
PubMed1984

Parasitic infection, nutrition, and immune response.

Parasites differ enormously in their abilities to evade normal host defenses. Intracellular protozoa are capable of surviving and multiplying within phagocytes and other cells whereas most nematodes do not multiply within the host. Both T lymphocyte-mediated immune responses and antibody production are important in limiting parasite invasion and in eliminating them. Of the nonspecific factors, macrophages, natural killer cells, and nonantibody serum factors can cause damage to parasites. Malnutrition impairs immunity, most notably cell-mediated processes. The number of T lymphocytes is reduced and there are significant alterations in T cell subsets. Mucosal antibody response is blunted, complement activity is decreased, and microbicidal capacity of phagocytes is reduced. Such changes in host resistance are important determinants of the final outcome of host-parasite interactions.

Antibody Formation↗
PubMed1983

Numerical and functional deficiency of suppressor T cells precedes development of atopic eczema.

Immunoregulatory T cells were studied quantitatively and functionally at age 1-2 months in 30 symptom-free infants with family history of atopic disease and in 30 infants with no such history. The infants were followed up for 24-37 months (mean 28.2 months) to see whether clinical atopic disease was expressed. In infants in whom atopic eczema subsequently developed, numbers of T8-positive cells were reduced, the T4/T8 ratio was raised, and functional suppressor activity was lower than normal. These findings indicate that a defect of T-cell regulation precedes clinical atopic disease and is of primary pathogenetic importance.

Antibodies, Monoclonal↗
PubMed1983

Nutrition and immune responses.

Clinical and epidemiologic data suggest a causal relationship between nutritional deficiency and infection. Among other factors, impaired immune responses secondary to malnutrition increase susceptibility to infectious illness. Protein-energy undernutrition and deficiencies of iron, zinc, pyridoxine, and other nutrients depress a variety of immunity functions. Cell-mediated immunity, complement system, microbicidal activity of phagocytes, secretory antibody response, and antibody affinity are often decreased. Recent studies have revealed many metabolic and hormone alterations as well as changes in the number and function of lymphocyte subpopulations. Obesity also is associated with impaired cellular immune functions. Dietary factors may play a critical role in host resistance to disease.

Age Factors↗
PubMed1982

Double-blind controlled crossover trial of 4% intranasal sodium cromoglycate solution in patients with seasonal allergic rhinitis.

In a double-blind, controlled, crossover study involving 47 subjects documented with seasonal allergic rhinitis, repeated intranasal administration of 4% sodium cromoglycate solution was associated with significant reduction in symptoms and decrease in consumption of antihistaminic drugs. Side effects were mild and transitory. It is concluded that intranasal sodium cromoglycate administration is an efficacious preventive and therapeutic approach in the management of patients with seasonal allergic rhinitis.

Administration, Intranasal↗
PubMed1981

Serum thymic hormone activity in genetically-obese mice.

1. Serum thymic hormone was assayed in genetically-obese (C57B1/6J ob/ob) mice and lean controls (+/+, +/-) of the same strain. 2. The thymic hormone activity was higher in the majority of the obese animals compared with non-obese mice. 3. The number of antibody-forming cells in the spleen expressed as a proportion of the total mononuclear cells was increased in the obese mice. 4. It is suggested that obesity is associated with significant changes in the thymic hormone levels which may alter the relative proportion of lymphocyte subsets and cell-mediated immunity.

Animals↗