It has been proposed that a zinc deficiency induces a relative decrease in T-helper type 1 immune response, therefore promoting the T-helper type 2 response, a key feature of asthma immunopathology. In order to verify the hypothesis that a zinc deficiency may cause a T-helper type 1/T-helper type 2 imbalance resulting in increased eosinophil inflammation, we used a murine model in which BALB/c mice were intraperitoneally sensitized (8 μg on day 0 and day 5) and challenged with nebulized ovalbumin (0.5% ovalbumin on day 12). Zinc-deficient mice were given a special zinc-free diet for 4 weeks prior to sensitization and ovalbumin challenge. The zinc-deficient group was compared to the normal-diet group and to a zinc-supplemented group in which animals were administered a zinc supplement added to the water supply. Two days after challenge, BAL was performed and the animals were killed for histologic evaluation of the lungs. This model was found to induce a significant level of bronchopulmonary eosinophilia as documented by the presence of 20 ± 1% eosinophils in the BAL cell counts (n = 57). A 35% increase in BAL eosinophils was observed in the zinc-deficient group (p < 0.05, n = 25), consistent with the increase in eosinophils found in the perivascular and peribronchial regions of the lung. In contrast, zinc supplementation was found to decrease BAL eosinophils by 34% (p < 0.05, n = 26), whereas dexamethasone (5 mg/kg intraperitoneally administered 30 min before ovalbumin challenge) induced a 59% decrease in BAL eosinophils in the same model. This study clearly showed that zinc deficiency increases allergic eosinophilic inflammation, whereas dietary zinc supplementation attenuates its intensity. Research looking into the potential benefits of long-term zinc supplementation in asthmatic patients is currently being undertaken.