Clinical enhancement of nutritional immunity.
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With reference to the studies carried out in the Center of Hematology, Bucharest, the authors review recent publications concerning the correlation between iron metabolism and infection, and emphasize the importance of iron deficiency within the framework of nutrition-infection-immunity relationship, and the role of iron in antinfectious defence. Among the metabolic responses of the host organism to infection is the early redistribution of essential oligoelements, known as "nutritional immunity", which is discussed in detail. Data refering to the leukocytic endogenous mediator are given.
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Clinical and epidemiologic data point to a causal interrelationship between nutritional deficiency and infectious illness. Both are major contributors to childhood morbidity and mortality, particularly in underprivileged population groups. Energy-protein undernutrition and deficiencies of iron, folates and pyridoxine, depress a variety of immunity functions. Delayed hypersensitivity and number of T lymphocytes are consistently reduced. In small-for-gestation low birth weight infants, cell-mediated immunity may remain depressed for several years. B lymphocytes, immunoglobulin levels and antibody responses are generally normal, but secretory IgA-antibody is reduced. Serum complement components are low and there is evidence of in vivo consumption of complement C 3. Neutrophil phagocytosis of bacteria and fungi is intact but the next step of intracellular killing is impaired. There are changes also in the production of lysozyme and interferon. Infection per se results in nutrient losses, either actual or by sequestration, and produces immunosuppression. The correction of postnatal nutritional deficits and/or infection is associated with reversal of immunological functions to normal. The interplay of nutrition, immunity and infection, and its biological implications are described.
In a previously healthy 13-year-old girl with disseminated blastomycosis, immunodeficiency was considered because of lymphopenia and the slow response of her lung disease to therapy with amphotericin B. Cellular immunity was found to be profoundly impaired, with absent delayed cutaneous hypersensitivity to several common antigens, a decreased count of thymus-dependent lymphocytes in the peripheral blood and a greatly diminished in-vitro proliferative response of lymphocytes to phytohemagglutinin (PHA). Humoral immunity was intact. Two additional types of therapy were assessed: subcutaneous injection of transfer factor was associated with an unsustained increase in lymphocyte counts and a positive cutaneous response to PHA but no clinical change; parenteral alimentation to ensure an adequate energy intake was associated with rapid clinical improvement, the development of delayed hypersensitivity to four additional antigens, and the return of lymphocyte counts and proliferative response to normal. These findings suggest that increased energy intake rather than transfer factor therapy was responsible for the child's recovery, and they emphasize the importance of adequate nutrition in the maintenance of intact cellular immunity.
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An important component of nonspecific defense of vertebrates against microbial invasion is that of nutritional immunity. Hosts attempt to withhold growth-essential iron from invading bacteria, fungi, and protozoa. Clinical conditions in which hosts are stressed by excess quantities of iron in specific fluids, tissues, or cells result in enhanced susceptibility to infection. Methods for strengthening nutritional immunity are known in theory; research is needed to determine if these would be useful in clinical practice.
This compacted overview of the nutrition-immune response connection underscores the role of nutrition as a deterrent to infection. Malnutrition enhances the propensity to and heightens the intensity of infections by weaknening the various host defense mechanisms. Thus: 1. Deficiencies of vitamin A, niacin, riboflavin, folic acid, vitamin B12, pyridoxine, ascorbic acid, iron and protein disrupt the tissue barriers to infection. 2. Protein-calorie, folate, iron, pyridoxine and zinc deprivations markedly depress the cell-mediated immune system. 3. Deficiencies of protein, pyridoxine, folic acid, pantothenic acid, thiamine, biotin, riboflavin, niacin-tryptophan, vitamin A and ascorbic acid inhibit humoral antibody formation in mammalian systems. 4. Vitamin A lack prevents the formation of lacrimal, salivary and sweat gland lysozymes. 5. Complement, properdin, interferon and transferrin concentrations are reduced in those nutritional deficiencies that interfere with protein synthesis. 6. Protein-calorie, iron and folate deficiencies impair phagocytosis by interfering with phagocyte microbial killing power or with phagocyte production. 7. Protein, ascorbic acid and zinc deficiencies retard wound healing that prevents spread of infectious lesions.
Nutritional deficiency reduces antibody synthetic capacity. Antibody directed against tumor antigens, however, may serve either to heighten tumor immunity, as in antibody-dependent cellular cytotoxicity, or to diminish host resistance to cancer growth by "blocking" cell-mediated tumor immunity. Diets made deficient in specific amino acids are inimical to tumor growth, apparently through reduction of synthesis of blocking antibody. Thus, where tumor immune function is involved, complex and possibly paradoxical effects of nutritional status on tumor growth can be predicted.
Protein-calorie malnutrition leads to depression of host cell-mediated immunity. Nutritional repletion initially results in rapid weight gain followed by a more gradual return of immunocompetence. Administration of a synthetic amino acid diet to normal animals did not preserve body weight or cell-mediated immunity any better than did a high carbohydrate, protein-free diet. Administration of a synthetic amino acid diet to malnourished animals maintained body weight, but did not restore immunocompetence. Proper nutritional repletion should provide both adequate protein and nonprotein calories if a return of immunocompetence is to be anticipated.
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The gastrointestinal tract hosts a complex community of microorganisms and helminth parasites that collectively contribute to host health and fitness. Analysis of these communities provides insight into diverse aspects of host dietary ecology, immunity, nutrition, and host-parasite interactions. However, research methodologies, such as sample preservation and sequencing approach, can influence how we understand and characterize these features. Here, we profiled the gastrointestinal microbial and helminth communities in different groups of wild Costa Rican mantled howler monkeys (Alouatta palliata palliata). We compared samples stored in ethanol versus directly flash frozen, and contrasted conclusions drawn from 16S versus shotgun sequencing approaches. Bacterial, archaeal, and eukaryotic taxa associated with the digestion of plant material dominated the GI communities. Storage and sequencing methods influenced microbial profiles: ethanol-stored samples exhibited higher diversity than frozen samples, and 16S sequencing detected lower diversity than shotgun. Helminths were detected via coprological microscopy in 71% of individuals, whereas metagenomic detection was inconsistent. This study provides new data on the microorganisms and their putative digestive functions in the gut of a folivorous primate, and highlights the pros and cons of different methodological choices when profiling host-microbiome and host-parasite interactions.