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[Iron and infection. I. Iron and "nutritional immunity". The leukocytic endogenous mediator].

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.

Adolescent↗
PubMed1979

Interactions of nutrition, infection and immune response. Immunocompetence in nutritional deficiency, methodological considerations and intervention strategies.

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.

Antibody Formation↗
PubMed1978

Cellular immunity and nutrition in refractory disseminated blastomycosis.

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.

Adolescent↗
PubMed1977

Infection and iron metabolism.

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.

Animals↗
PubMed1979

Nutrition and the immune response -- a review.

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.

Animals↗
PubMed1978

Effects of protein depletion and repletion on cell-mediated immunity in experimental animals.

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.

Amino Acids↗
PubMed2026

Ecological and methodological insights from genetic and coprological profiling of gastrointestinal communities in wild howler monkeys.

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.

Animals↗
PubMed2026

Genomic analysis of Neisseria gonorrhoeae strains from disseminated, urogenital, and rectal infections reveals differences in genes for iron acquisition and type IV secretion.

Neisseria gonorrhoeae, an obligate human pathogen, causes the sexually transmitted infection gonorrhea. Delayed treatment or immunodeficiencies can result in a higher risk of disseminated gonococcal infection (DGI), where the infection spreads to normally sterile anatomic sites, including the bloodstream. The gonococcus produces TonB-dependent transporters (TdTs) to sequester metals from host nutritional immunity proteins. These transporters are critical for survival and are important virulence factors. We characterized genes encoding iron-regulated TdTs in the genomes of strains from disseminated (n = 47), urogenital (n = 86), and rectal (n = 12) infections. We found that gonococcal strains isolated from DGI infections were more likely to express a functional hemoglobin-iron utilization operon (hpuAB wild type and phase on [32%, n = 15/47]), to harbor nonsense mutations in tdfF (57%, n = 27/47), and were predicted to express low levels of fetA (43%, n = 20/47) when compared to strains from urogenital or rectal infections. In contrast, gonococcal strains from localized urogenital infections were associated with a higher frequency of functional tdfF genes (66%, n = 57/86) and high fetA expression (30%, n = 26/86). Additionally, strains from rectal infections were more frequently found to have high fetA expression (33%, n = 4/12) and a functional tdfF (75%, n = 9/12). Furthermore, we identified associations between the presence and absence of tdfF and the gonococcal genetic island, which encodes a type IV secretion system. These findings inform our evolving understanding of the molecular mechanisms underlying disseminated gonococcal infections.IMPORTANCEGonorrhea is an emerging, global health threat, with over 100 million new cases each year. Delayed treatment, immunosuppressive medications, and immunodeficiencies can contribute to the spread of infection to the blood, presenting as a serious disseminated manifestation. With rising antimicrobial resistance and no licensed preventative vaccine, untreatable gonorrhea is a possibility in the near future. TonB-dependent transporters are highly conserved and vital for metal acquisition and survival, making them promising targets for therapeutic or preventative strategies. Associated surface-exposed lipoproteins display greater sequence variation but contribute to metal acquisition. We analyzed the genes encoding TonB-dependent transporters and associated lipoproteins from strains associated with distinct disease manifestations. We conclude that gonococci isolated from disseminated, urogenital, and rectal sites demonstrate different phase and allelic variations in genes encoding iron transport systems and the gonococcal genetic island.

Humans↗
PubMed1976

[Considerations regarding the influence of intrauterine and early postnatal diseases and nutritional deficiencies on immunity and disease epidemiology (author's transl)].

Malnutrition, infectious and toxic stress, hormonal and enzymatic deficiencies as well as graft versus host reactions during the last trimester of pregnancy and during the first six months of life lead to persistent depressions of cell mediated immunity. The subsequent imbalance between the cell mediated and humoral system of immunity leads to differences in disease prevalence in poor and rich populations. Particularly leprosy, tuberculosis, viral disease as for instance frequently fatal measles and diseases due to complexes between humoral antibody and bacterial components as for example acute rheumatic fever occur with increased frequency in B (+) T (-) populations. Desturbances of immune surveillance due to suppression of specific cell mediated immune function leads to an increased frequency of neoplasia, particularly B-cell lymphoma and gastrointestinal tumors. Populations in which the T-cell system can mature without interference show a trend towards diseases in which excessive T-cell response plays a major role, as for instance rheumatoid arthritis, Sjögren syndrome, terminal ileitis, autoimmune angiopathies, multiple sclerosis and possibly also disseminated lupus erythematodes.

Autoimmune Diseases↗
PubMed1979

[The effect of parenteral nutrition on cellular immune status in patients with gastrointestinal cancer].

In a pilot study, the distribution of lymphocyte subpopulations in the peripheral blood and skin tests with recall antigens have been examined in 42 patients with gastrointestinal cancer before and during a perioperative parenteral hyperalimentation. Concerning the calories and the concentrations of amino acids and carbohydrates, two different solution regimens were applied. During parenteral nutrition with 2400 and 2200 kcal especially the absolute numbers of lymphocyte subpopulations increase reflecting the changes of total lymphocyte count. There was no marked difference between the 2 groups. Both solutions are qualified to balance the preoperative catabolic situation indicated by preoperative lymphopenia. This kind of parenteral nutrition did not influence the patient's cellular immunological status which was tested by 3 recall antigens. It must, however, be considered that the physical i.e. nutritional situation of the patients was not reduced to an extent where the immunological status was impaired. Our results suggest that in the perioperative period cancer patients should be supported by hypercaloric parenteral nutrition. On the other hand more sensitive immunological tests such as DNCB for skin testing and functional assays for in vitro tests are necessary to assess the effects of this kind of therapy.

B-Lymphocytes↗
PubMed1978

Nutrition and the immune response.

Vitamin E--selenium deficiency in dogs resulted in complete suppression of lymphocyte responsiveness to stimulation with mitogens. Depressing effects on neutralizing antibody synthesis were also noted. A serum factor associated with the inability of lymphocytes to respond has been isolated and partially purified. The suppressor factor can be removed or transformed by both in vivo and in vitro vitamin E supplementation.

Animal Nutritional Physiological Phenomena↗