*Karen Sellins is a senior research associate and Dr. Terry Engle is an assistant professor of ruminant nutrition at Colorado State University. To expedite answers to questions concerning this column, please direct inquiries to Feedstuffs, Bottom Line of Nutrition, 5810 W. 78th St., Suite 200, Bloomington, Minn. 55439, or email firstname.lastname@example.org.
THE interactions between trace minerals and disease resistance are extremely complex, and many factors can affect an animal's response to trace mineral supplementation.
These factors include the duration and concentration of trace mineral supplementation, physiological status of an animal, absence or presence of dietary antagonists, environmental factors and stress.
Minerals can be broken down into four functional categories:
1. Structural minerals play a role as components of tissues;
2. Physiological minerals are involved in acid-base balance;
3. Catalytic minerals are components of enzyme and hormone systems, and
4. Regulatory minerals are involved in cell replication processes (Underwood and Suttle, 1999).
Zinc, copper and selenium fall mainly into the catalytic and regulatory categories. Deficiencies and/or imbalances of trace minerals can alter the activity of certain enzymes and the function of specific organs, thus impairing specific metabolic pathways as well as overall immune function.
For in-depth reviews of the effects of micronutrients on immunity, refer to Galyean et al. (1999) and Spears (2000).
Immunity is the ability to resist infection (Kuby, 1994) and can be classified into two components: nonspecific (innate) and specific (adaptive) immunity.
Nonspecific immunity refers to the basic resistance to disease that a species possesses. Nonspecific immunity includes four types of defensive barriers: (1) anatomic/skin, (2) physiologic — temperature, pH or oxygen tension, (3) phagocytic or the ingestion of macromolecules by macrophages and neutrophils and (4) inflammatory or vasodilatation and capillary permeability (Kuby, 1994).
Specific immunity is immunity induced by exposure to an antigen, either naturally or via vaccination (Kuby, 1994). Specific immunity can be further divided into two branches: humoral and cell-mediated immunity.
The humoral branch of the immune system involves antigen-specific B cells that proliferate, differentiate and secrete antibodies upon interaction with their specific extracellular antigen. These antibodies are the effector molecules of the humoral response as they bind to extracellular pathogens and facilitate their elimination.
Cell-mediated immunity involves the direct interaction of specific T cells with infected cells to eliminate intracellular pathogens (Galyean et al., 1999).
Trace minerals and immunity
Zinc. Numerous experiments with humans and laboratory animals have indicated that zinc deficiency reduces immune response and disease resistance (Chesters, 1997). However, there is limited research in ruminants examining the influence of zinc deficiency on immune function and disease resistance (Spears, 2000).
Lambs fed a semi-purified diet severely deficient in zinc showed a reduced in vitro T cell growth response to a mitogen (a substance that stimulates proliferation) but an increased B cell growth response to a mitogen that relies on T cells (Droke and Spears, 1993). Zinc-deficient lambs also had a lower percentage of lymphocytes and a higher percentage of neutrophils (phagocytic cells). The inflammatory response by T cells was similar in zinc-adequate and zinc-deficient lambs.
Furthermore, zinc-deficient cattle showed similar cell-mediated and humoral immune responses to zinc-adequate cattle (Spears and Kegley, unpublished data).
However, Engle et al. (1997) reported a greater skin swelling response to a subdermal antigen injection in zinc-adequate calves compared to marginally zinc-deficient calves.
Zinc supplementation has been associated with an increased antibody response and a decrease in respiratory disease in feedlot steers (George et al., 1997). This may be due to the function of the copper-zinc superoxide dismutase enzyme or to an increase in a variety of other immune processes that involve zinc as well (Hambidge et al., 1986).
Copper. Copper is an essential element that is required for an array of metabolic functions, including iron metabolism, cellular respiration (energy production), cross-linking of connective tissue, central nervous system formation, reproduction and immunity, as well as several other functions (McDowell, 1992).
Severe copper deficiency induced by feeding a semi-purified diet low in copper did not affect in vitro mitogen-induced B and T cell proliferation in cattle (Stabel et al., 1993; Ward et al., 1997).
Furthermore, the addition of 5 mg/kg of molybdenum to the semi-purified diet to produce a more severe copper deficiency did not reduce B and T cell proliferation to mitogens (Ward et al., 1997).
However, Wright et al. (2000) indicated that a low copper status in steers was associated with a reduced response of T cells to mitogens following weaning and an infectious bovine rhinotracheitis virus (IBRV) challenge.
Selenium. Since its discovery by Rotruck et al. (1973), selenium has been shown to affect specific components of the immune system.
Earlier research by Reffett et al. (1988) reported lower serum immunoglobulin M — an antibody produced by B cells — concentrations and anti-IBRV levels in selenium-deficient calves challenged with IBRV than in selenium-adequate calves.
Neutrophil function was reduced in goats (Aziz et al., 1984) and cattle fed selenium-deficient diets compared with controls receiving selenium-adequate diets.
Some studies have shown increased T cell proliferation following in vitro stimulation with mitogens, while others have not (Spears, 2000).
The Bottom Line
The interactions among trace minerals, immunology and disease resistance are extremely complex. From the more basic molecular immune research, it is clear that trace minerals play an important role in the immune response.
Despite the apparent involvement of certain trace minerals in the immune system, trace mineral deficiencies have not always increased the susceptibility of domesticated livestock species to natural or experimentally induced infections (Spears, 2000).
Many factors could affect an animal's response to trace mineral supplementation — such as the duration and concentration of trace mineral supplementation, the physiological status of an animal, the absence or presence of dietary antagonists, environmental factors and the influence of stress on trace mineral metabolism — and may depend on the class of immune cell being studied (Dorton et al., 2003).
Portions of this this article were published previously in other publications.
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