Contribution of Basophil/Mast Cell and Eosinophil Growth and Differentiation to the Allergic Tissue Inflammatory Response

The mechanisms underlying allergic tissue basophil/mast cell (BMC) or eosinophil (Eo) accumulation are unclear, especially since chemotaxis or IgE levels do not offer a sufficient explanation. We have found that a formaldehyde-blockable, steroid-responsive nasal metachromatic cell (NMC) population predominates in epithelium and correlates well with symptoms and signs in patients with allergic rhinitis. Circulating BMC and Eo progenitors (colony-forming cells in culture; CFU-c) are increased in atopic patients, inversely related to NMC counts, and fall as NMC numbers rise during seasonal allergen (ragweed pollen) stimulation. The metachromatic cell progeny of these CFU-c are also formaldehyde-blockable in their staining reaction and thus may correspond to NMC. Human nasal polyps yield BMC CFU-c. Nasal polyp epithelial scrapings or mononuclear cells, T lymphocytes or keratinocytes in vitro all produce potent BMC or Eo colony-stimulating activities (CSA) as well as an interleukin-3-like activity, each of which is partially separable from the others. Nasal epithelial cells cultured from scrapings of atopic, as opposed to nonatopic, patients also produce BMC or Eo CSA with an enhanced effect of the former on atopic peripheral blood CFU-c growth. These studies support the hypothesis that BMC and Eo accumulate in allergic inflammation as a result of in situ growth and differentiation of progenitors stimulated by soluble hemopoietic factors derived from mucosal cell populations.