Sephadex G-200-induced eosinophil infiltration into airways in non-sensitized and sensitized guinea pigs, and responsiveness of the cells to stimuli in vitro.

Eosinophils are thought to be one of the pathophysiologically pivotal cells in atopic-type inflammation. In the present experiments, the in vitro responsiveness to stimuli of eosinophils, which had infiltrated into the airway following intravenous administration of Sephadex G-200 (Sephadex), was mainly studied in non-sensitized and [antigen + Al(OH)3]-sensitized guinea pigs. In sensitized, Sephadex-treated guinea pigs, a large number of eosinophils were found in the bronchoalveolar lavage fluid, whereas a much smaller number of cells were recovered in either non-sensitized or sensitized, Sephadex-untreated animals and a smaller number were recovered in non-sensitized Sephadex-treated animals. The eosinophils from non-sensitized Sephadex-treated guinea pigs released superoxide anion (.O2-) and thromboxane (TX) B2 in response to platelet-activating factor (PAF), leukotriene B4 and Ca ionophore A23187. Either spontaneous or PAF-induced .O2- generation from eosinophils of sensitized, Sephadex-treated guinea pigs was significantly greater than that from non-sensitized animals, while TXB2 release stimulated by any of the above stimuli was not further enhanced by sensitization. These results indicate that active sensitization can change some eosinophil functions and that the functionally altered cells could play a pathophysiological role in atopic inflammation.