The need for effective immune function for the maintenance of health has been clearly established in both agriculturally significant animal species and humans. Intensive agricultural practices present production species with numerous disease challenges during the rearing period. Environmental factors represent a ubiquitous, yet frequently manageable, category of immunomodulators that can influence immune performance and ultimately disease susceptibility or resistance. However, strategies for assessing overall immune potential have not been widely implemented for agricultural species. This is in contrast to the use of immune evaluation for human health considerations. Immune assessment relative to environmental-immune interactions can produce benefits in two areas. First, the efficiency of the production operation can be enhanced. Second, the welfare of the animals during the production cycle can be optimized. This paper presents an overview of environmental factors known to influence the immune function of poultry and the opportunities to manage environmental factors to benefit the health of the animals. In addition, the paper discusses the status of immunological assessment for humans and laboratory animals and proposes potential immune assessment panels that could serve as a tool to optimize the environmental management of poultry populations.
Lead has been shown to exert toxic effects during early development. In these in vivo and ex vivo experiments, the effect of lead on the immune system of the developing embryo was assessed. Nine-week-old female Fischer 344 rats were exposed to lead acetate (0, 100, 250, and 500 ppm lead) in their drinking water during breeding and pregnancy (exposure was discontinued at parturition). Offspring received no additional lead treatment after birth. Immune function was assessed in female offspring at 13 weeks of age. Dams in lead-exposed groups were not different from controls with respect to the immune endpoints used in these experiments; however, in the offspring, lead modulated important immune parameters at modest exposure levels. Macrophage cytokine and effector function properties (tumor necrosis factor-alpha and nitric oxide production) were elevated in the 250 ppm group, while cell-mediated immune function was depressed, as shown by a decrease in delayed-type hypersensitivity reactions in the 250 ppm group. Interferon-gamma levels were decreased in the 500 ppm treatment group. Serum levels of IgE were increased in rats exposed to 100 ppm lead. These results indicate that exposure of mothers to moderate levels of lead produces chronic immune modulation in their F344 rat offspring exposed in utero. Since the mothers were not susceptible to chronic immune alterations, a developmental bias to the immunotoxic effects of lead is indicated. The differences observed are consistent with the possibility that lead may bias T helper subset development and/or function, resulting in alterations in the balance among type 1 and type 2 immune responses.
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