Reproduction of the eosinopenia of acute infection by passive transfer of a material obtained from inflammatory exudate.
Studies of the eosinopenic effect of acute inflammation were conducted in mice previously rendered eosinophilic with trichinosis. Exudate removed from a pneumococcal abscess contained material (eosinopenic factor [EF]) capable of causing eosinopenia of 4- to 24-h duration when injected intraperitoneally into eosinophilic mice. The material passed through a 0.45-micronm filter, but was retained by a dialysis membrane capable of retaining protein molecules of greater than approximately 30,000 molecular weight. EF was soluble in 7% perchloric acid, was not destroyed by pneumococcal proteolytic enzymes in the presence of Trasylol, but was inactivated by heating to 56 degrees C for 30 min. EF was detectable in the exudate after 10 h and had reached its highest concentration after 20 h. When the effect of EF was expressed as a percent suppression of control eosinophil levels, there was a geometric dose response. Eosinopenia could not be ascribed to steroids present in the preparation, and the EF was effective in adrenalectomized animals. Eosinopenia was not induced by transfer of similarly treated heat-killed pneumococci, pneumococcal culture filtrate, or normal serum. The eosinopenia of acute infection may be the direct effect of a substance present at the site of acute inflammation.
Reproduction of the eosinopenia of acute infection by passive transfer of a material obtained from inflammatory exudate. Studies of the eosinopenic effect of acute inflammation were conducted in mice previously rendered eosinophilic with trichinosis. Exudate removed from a pneumococcal abscess contained material (eosinopenic factor [EF]) capable of causing eosinopenia of 4- to 24-h duration when injected intraperitoneally into eosinophilic mice. The material passed through a 0.45-micronm filter, but was retained by a dialysis membrane capable of retaining protein molecules of greater than approximately 30,000 molecular weight. EF was soluble in 7% perchloric acid, was not destroyed by pneumococcal proteolytic enzymes in the presence of Trasylol, but was inactivated by heating to 56 degrees C for 30 min. EF was detectable in the exudate after 10 h and had reached its highest concentration after 20 h. When the effect of EF was expressed as a percent suppression of control eosinophil levels, there was a geometric dose response. Eosinopenia could not be ascribed to steroids present in the preparation, and the EF was effective in adrenalectomized animals. Eosinopenia was not induced by transfer of similarly treated heat-killed pneumococci, pneumococcal culture filtrate, or normal serum. The eosinopenia of acute infection may be the direct effect of a substance present at the site of acute inflammation.