Effect of zinc deficiency on humoral and cell-mediated immunity

Typescript (photocopy).The effects of dietary zinc deficiency on humoral and cellular immunity, as well as the functional significance of zinc deficiency on host responses to infection with a facultative intracellular pathogen, were studied in female, specific pathogen-free rats. The plaque-forming capacity of spleen cells and hemolytic antibody titers in serum were measured in rats maintained on a zinc-depleted or normal diet for periods of the time ranging from 3 to 10 weeks and immunized with srbc six days prior to sacrifice. The in vitro response of splenic lymphocytes to a polyclonal T-cell mitogen was also investigated. Hemolysin titres and plaque-forming cells per million spleen cells were not affected by zinc deficiency. A cell-mediated immune malfunction was evidenced by impaired lymphocyte blastogenesis following stimulation with a T-cell mitogen, phytohemagglutinin (PHA). In order to assess the response to an infectious disease, animals receiving either the low zinc or normal diet for six, eight or ten weeks, to establish a chronic deficiency, were challenged with Listeria monocytogenes five days prior to sacrifice. Zinc-deficient rats demonstrated thymic atrophy, reduced delayed hypersensitivity responses to listeria antigen, larger bacillary loads in some tissues, and impaired lymphocyte response to PHA but not to Concanavalin A. Half of the rats given the zinc deficient or the control diets for six weeks were vaccinated with viable Listeria monocytogenes and 10 days later all rats were challenged via the respiratory route with L. monocytogenes. Five or six days later the animals were skin tested and sacrificed. Vaccination resulted in control of bacteria and decreased delayed hypersensitivity in both dietary groups at six days post-challenge. Vaccinated animals fed the zinc-adequate diet had significantly higher stimulation indexes to PHA than non-vaccinated and zinc-deficient vaccinated animals. In sum, chronic, moderate zinc deficiency produces thymus involution and impaired response to a polyclonal mitogen. Primary antibody response to srbc immunization was not affected and although zinc-deficient animals had larger bacillary loads in tissues when infected with Listeria monocytogenes, upon vaccination they were able to control the infection as well as control animals