Dr.Paola Persico
Recent studies have now confirmed as immunology and nutrition are closely related. Many substances such as arginine, glutamine, zinc, Omega-3 fatty acids and nucleotides improve the cellular immunity, modulate the metabolism of cancer cells and promote clinical recovery.
TRACE ELEMENTS AND IMMUNITIES
The lack of trace elements such as zinc, copper, iron, selenium and vitamins adversely affect normal immune responses in the body at conception. The development of the immune system is implemented mainly in the womb and shortly after birth. The deficiencies of certain minerals, such as zinc, copper, essential amino acids, vitamin A, can affect the development of growing animals and their immunocompetence for both adaptive immune responses that for those innate.
Maternal zinc deficiency during pregnancy can affect the normal reaches the number of thymic and splenic lymphocytes in puppies (Table 1). Zinc is in fact essential for the normal development and activity of cells responsible for immunity nonspecific as well as neutrophils and natural killer cells.
A deficiency of zinc also influence the normal onset of immunity acquired (such as the activation and development of T lymphocytes, cytokine production, and B cell antibody production, particularly the production of immunoglobulin G is compromised). The effects of zinc are also found in the fundamental functions of the cell (such as DNA replication, transcription of the RNA, the division and the cell activation). Zinc is also considered an antioxidant and stabilizer of the membranes.
States of malnutrition during the uterine development may affect the normal development of intestinal microflora with an alteration, even permanent, of the enteric mucosal response with increased susceptibility to infection. This type of mucosal alteration can persist even for the whole life of the subject
| Nutrients | What causes their deficiency (examples) |
| Zinc | Lack of development of the thymus, alterations in the differentiation of T lymphocytes, reduced production of cytokines by Th1, decrease in antibody production |
| Copper | Decreased lymphocyte proliferation |
| Selenium | Increased susceptibility to infection |
| E Vitamin | Increased production of PGE2 |
OBESITY AND IMMUNITY
Episodes of prolonged fasting can affect the normal development of lymphoid organs with atrophy, decrease in the number and function of circulating leukocytes, etc. the final result is a decrease in the ability to respond to infections. Numerous studies have been conducted in Human Medicine to evaluate the correlation between efficient immune response and obese patient. In domestic animals, except rodents, and are often the first link in humans for experimental studies, no study has yet allowed to clearly correlate immune function and obesity. In obese subjects, in human medicine, decreased lymphocyte responses were seen after the antigenic stimulation, reduced natural killer cell function, imbalance of the ratio CD8: CD4 and altered neutrophilic capacity. In humans, studies have shown that obesity is closely related to an increase in both the concentration of circulating inflammatory cytokine produced by macrophages activated by excess adipose tissue, that of acute phase proteins.
INFECTIONS AND NUTRITION
While conditions such as prolonged fasting and / or obesity can impair the body’s normal immune response is also true that the immune responses to infections, malignancies or severe immune-mediated diseases may compromise the nutritional status of the organism.
In case of serious infection and / or sepsis conditions, for example, there is a loss of appetite which may bring even to anorexia. In these patients there is an increase of inflammatory cytokines, particularly IL-1, IL-6 and TNF-alpha, which act on the central nucleus of the hypothalamus and peripheral nervous system lead to lower/ suppression of food intake. The activation of inflammatory cytokines seems to be a protective hand to the body while the other causes a loss of lean body mass, fat and a lack of nutrients. Following a tumor episodes of prolonged fasting can occur, accompanied by body adaptations that ensure the survival of the vital organs, but also to cachexia.
CACHEXIA, AND OMEGA 3 FATTY ACIDS
Cachexia can be defined as a set of factors that determine alterations in lipid metabolism, protein and glucose resulting in loss of weight and deterioration of the organic conditions and quality of life in patients with cancer. What link the pathogenesis of cancer cachexia, which is considered a multifactorial problem, is the protein-muscle catabolism (resulting in lean mass loss) induced by the increase of various cytokines and that induces production of acute phase proteins (such as the C-reactive protein). Today in Human Medicine is attributed to this mechanism to the production, by the neoplastic cells, a substance the “proteolysis-inducing factor” (PIF proteolysis Inducing Factor). This factor acts stealing proteins to the muscles to supply the tumor and is reducible by administering eicosapentaenoic acid (EPA).
The neoplastic tissue seems to preferentially draw their nutrition from glucose as an energy source of choice, then forcing the neoplasia to use other energy substrates (such as fats and proteins) would help to reduce cell proliferation. The use of certain amino acids (arginine, glutamine, leucine, valine, etc.) compared to other seems useful to retard tumor growth. In studies performed in animal models it has been shown that the increased intake of omega-3 fatty acids can interfere with the growth rate of certain cancers. In fact it seems that EPA and DHA may attenuate tumor growth thanks to their ability to decrease the metabolism of arachidonic acid.
Some studies conducted in vivo, have shown that EPA has a selective effect on tumor cells carrying them to death. Further research has shown that the administration of omega-3 reduces the secretion of TNF-alpha factor, interleukin 1-alpha and interleukin-2, which are important mediators of the cachectic process and also play a fundamental role as factors of tumor growth.
NUCLEOTIDES AND IMMUNITY
A number of recent studies have focused on the role of exogenous nucleotides as regulators of the immune response. The nucleotide is the basic unit of nucleic acids, phosphoric acid is formed, from a monosaccharide pentose which is the ribose for RNA and deoxyribose for DNA and from nitrogenous bases (adenine, guanine, cytosine, uracil for l ‘RNA and adenine, cytosine, guanine and thymine for DNA). The body requires constantly nucleotides, especially for situations with a high turnover of cell turnover, as the immune system. Although the nucleotides can be synthesized endogenously, when internal production drops then becomes necessary intake via the alimentary channel. Most of the introduced nucleotide is rapidly metabolized and excreted; however, a certain amount is incorporated in the tissues. In such circumstances the nucleotides play a role defined as semi-essential.
From studies, it emerged that exogenous nucleotides are able to perform the important task of regulators of the immune response. Animal studies report that the introduction of the nucleotides in the diet stimulates the humoral response against T-dependent antigens, resulting in a total increase in antibody levels. The increase of immunoglobulins also enables improved vaccine response, increased tolerance towards food antigens a reduction in the overall morbidity.
Bibliography
- Ackerman L. “Nutritional supplements in canine dermatoses” Can Vet J 28: 29-33, 1987
- Becker WM, Hoekstra WG “The intestinal absorption of zinc” in “Intestinal Absorption Of Metal Irons, Trace Elements and Radionuclides”Skoryna SC, Waldron E. Oxford Press. 229-256; 1971
- Indian J Pediatr 2002 May; 69(5) 417-9 “Immunonutrition”Singh R, Gopalan S, Sibal A.
- 2.Acta Paediatr Suppl 1999 Aug, 88(430) 83-8 “Dietary nucleotides.effects on the immune and gastrointestinal systems” Carver JD.
- Chvapipl M “Effect of zinc on cells and biomembranes” Med Clin North Am 60:799, 1976
- Codner EC, Thatcher CD “Nutritional management of skin disease” Comp Cont Educ Pract Vet 15:411, 1993
- Cunnane SC “Differential regulation of essential fatty acid metabolism to the prostaglandins: Possible basis for the interactio of zinc and copper in biological systems” Prog Lipid Res 21:73, 1982
- Fernandes G, Nair M, Onoe K, Tanaka T, Floyd R, Good RA “Impairment of cell mediated immune functions by dietary. Zn deficiency in mice” Proc Nat Acad Sci, USA, 76: 457-61; 1979
- Kane E, Morris JG, Rogers QR,et al “Zinc deficiency in the cat” J Nutr 111: 488-95;1981
- Luecke RW, Simonel CE, Fraker PJ “The effect of restricted dietary intake on the antibody mediated response of the zinc deficient A/J mouse” J Nutr 108: 881-7; 1978
- Marsh KA, Ruedisueli FL, Coe S, Watson TDG “Effects of zinc and linoleic acid supplementation on the skin and coat quality of dogs receiving a complete and balanced diet” Veterinary Dermatology 11;277-284,2000
- Najin RA, Sharquie KE, Fariou IB “Zinc sulfate in the treatment of cutaneous leishmaniasis: study in vitro and in animal model “.Mem Inst OswaDlo Cruz, 39:1998
- National Research Council. “Nutrient Requirements of Dogs“. Washington, DC, National Academy Press, 1985
- Prasad AS “Zinc: mechanism of host defense” J Nutr, May, 137(5): 1345-9; 2007
- Prasad AS “Effects of Zinc Deficiency on Th1 and Th2 cytokine shifts” Journal of infectious Diseases, 2000; 182: S62-8
- Robertson BT, Burns MJ “Zinc metabolism and zinc-deficiency sindrome in the dog” Am J Vet Res 24:997; 1963
- Roudebush P, Sousa CA, Logas DE “Skin and hair disorders” Small An Clin Nutrition 4th ed. Marcelline: Walsworth Publishing 2000
- Roudebush P et al “Zinc responsive dermatosis in dogs” Vet Derm 13:63, 2002
- Scott DW, Miller Jr WH, Griffin CE “Muller & Kirk Small Animal Dermatology” 6th ed Philadelphia: Saunders 2001
- Shankar AH, Prasad AS “Zinc and immune function: the biological basis of altered resistance to infection” Am J Clin Nutr 68 (suppl): 447s-63s; 1998
- Watson TD “Diet and skin diseases in dogs and cats” J Nut 128 suppl 2783-9, 1999
