While growth retardation and reduced productivity are of economic importance, the intrinsic activity of many mycotoxins on the immune system of the animals is of increasing concern. The presence of moderate to low amounts of mycotoxins in daily feed rations increases the susceptibility of animals to viral, bacterial and parasitic diseases (Bondy and Pestka, 2000). This increased susceptibility requires increased therapeutic intervention with antibiotics and antiparasitic drugs. These interventions increase the costs for animal health care and the use of anti-infective agents, particularly antibiotics, at the farm level with a concomitant increase in the risk of induction and spread of antimicrobial resistance. The immu-nosuppressive effect of mycotoxins also may result in incomplete protection of farm animals following vaccination against viral diseases, as antibody formation is impaired. The impaired immune competence of animals following long-term exposure to mycotoxins has been hypothesized to facilitate the emergence and re-emergence of pandemic viral diseases in animals, including swine fever and avian influenza.
Measurable signs of impairment of innate immunity include the inhibition of phagocytosis by macrophages, the induction of an inflammatory response by different classes of cytokines, and activation of the complement cascade, which commonly follows exposure to various trichothecenes. The acquired immunity comprises B-lymphocyte-dependent immu-noglobulin production, as well as the activation of T lymphocytes. The response of the immune system to individual toxins varies. For example, aflatoxins affect primarily the cellular immune response to pathogens and phagocytic cell functions. Various experiments with chickens, but also with laboratory animal species, and ex vivo experiments with human and rodent cells show that aflatoxin Bj decreases the number of circulating T lymphocytes and splenic cell counts. It also reduces the phagocytic activity of the macrophages, reduces total complement activity, and decreases the production of pro-inflammatory cytokines. Inhibition of phagocytosis and reduced intracellular killing of pathogens make animals more susceptible to acute bacterial and fungal infections.
Ochratoxin A primarily affects the antibody-producing cells and decreases the synthesis of immunoglobulins. Impairment of cell-mediated immunity is associated with a decrease in circulating lymphocytes, monocytes and macrophages, and challenge experiments in immunized animals with specific pathogens, e.g., Pasteurella multocida, demonstrated the impaired acquired immunity following vaccinations. These effects also are observed in new-born animals that were exposed prenatally to ochratoxin A. Higher sensitivity of animals to a bacterial challenge with Listeria monocytogenes or Salmonella typhimurium also occurs following expo sure to T-2 toxin. T-2 toxin is a Type A trichothecene that affects bone marrow cells, resulting in a pancytopenia with reduced leukocyte counts, reduced blastogenic transformation of lymphocytes, and reduced response to mitogens of peripheral lymphocytes, thymic and spleen cells.
The immunomodulatory effects of deoxynivalenol and fumonisins remain the subject of intense research. Short-term exposure to deoxynivalenol seems to activate many immune functions, e.g., the expression of pro-inflammatory cytokines, while long-term exposure to moderate or low levels suppresses the response to pathogens and induces autoimmune-like effects, such as the production and renal disposition of IgA. Total IgM and IgG levels also decrease. Mitogen-induced lymphocyte proliferation is induced at low concentrations, but reduced at higher concentrations. A comparable time and dose-dependent deregulation of immune functions also is observed following fumonisin Bj exposure. Fumonisins induce the production of nitric oxide in various animal models with and without an LPS challenge. Nitric oxide is a strong vasodilator, which could contribute to the cardiovascular changes known to occur in pigs following exposure to fumonisin Bj, and to the leukoencephalomalacia seen in horses.
In conclusion, these few examples show that exposure to mycotoxins can both activate and suppress the immune system. General responses to mycotoxins, e.g., the modulation of cell proliferation, impairment of protein synthesis, induction of oxidative stress and induction of apoptosis also may contribute to the immunomodulatory effects of mycotoxins (for a review see Bouhet and Oswald, 2005).
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