COMPLEMENT RESISTANCE OF PATHOGENIC ENTAMOEBA-HISTOLYTICA MEDIATED BYTRYPSIN-SENSITIVE SURFACE COMPONENT(S)

Pathogenic forms of the protozoan parasite Entamoeba histolytica were reported previously to resist the cytolytic effect of the alternative complement pathway (AP) only temporarily during exposure to complement . In contrast, nonpathogenic forms of E. histolytica had been found to show AP resistance as a stable property. We studied the mechanisms of AP resistance of the two forms. Upon exposure to AP activity, resista nt pathogenic or nonpathogenic forms bound significantly less C3 produ cts than complement-sensitive pathogenic amebae, indicating that the t wo resistant forms both inhibited AP amplification. Various enzymatic treatments and inhibition of membrane mobility by cytochalasin B and g lutaraldehyde fixation showed that the mechanisms of AP inhibition dif fered between pathogenic and nonpathogenic forms; in contrast to nonpa thogenic forms, pathogenic amebae required intact membrane mobility an d a trypsin-sensitive surface component(s) to inhibit AP activation.