Experimental eosinophilia and inflammation--the effect of various inflammatory mediators and chemoattractants.

An experimental subcutaneous inflammation was produced in guinea pigs with peripheral blood eosinophilia. The eosinophilia resulted from two subsequent infections with Trichinella spiralis larvae. One group of guinea pigs served as non-infected control. Inflammation was induced by carrageenan, bradykinin, histamine, platelet activating factor and eosinophilotactic factors of lymphocytic or neutrophilic origin. Whereas in the control group no eosinophil granulocytic response was observed, this response was seen in the group with peripheral blood eosinophilia. The inflammatory substances and mediators (carrageenan, bradykinin, histamine, platelet activating factor) did not attract eosinophils alone, but also neutrophils. Under peripheral blood eosinophilia within the time course of the inflammatory reaction a second emigration with a shifted neutrophil/eosinophil ratio in favour of eosinophils was found. This could be due to a generation of chemoattractants by the injected substances themselves or more probably, by already emigrated granulocytes. Neither histamine, bradykinin, carrageenan, nor the eosinophilotactic factors (ECF's) in the concentrations used did release the cytotoxic major basic protein from eosinophils. Platelet activating factor exhibited a release of major basic protein from some eosinophils but no release of the peroxidase under our experimental conditions. The immigration of sufficient numbers of eosinophils into inflammatory areas might be one cause of the reduction of the inflammatory edema found in a previous investigation under similar conditions.