Human Chang liver cells show large surface openings and endocytic channels that resemble those in the amoeba.

Cytolysis of host cells by pathogenic Entamoeba histolytica can be blocked by specific lysozyme inhibitions and is recently reported to be enhanced by phosphoinositide (PI) signal transduction activation. However the mechanistic relationship between PI second messenger targets and massive lysosomal secretion needed to achieve rapid host cell lysis is unclear. We have previously shown that intracellular alkalinization associated with activated PI hydrolysis produces a massive endocytosis of huge proportions which would force a corresponding exocytosis for the maintenance of overall cell dimensions. These endosomes are processed by primary lysosomes. Apparently then, the massive exocytosis secretory pathway could provide the means for the ejection of lysozymes over target cells. We show here using human Chang liver cells that intracellular alkalinization produced large surface pittings similar to those seen in pathogenic E. histolytica in a rounded state. The SEM profile is correlated with the TEM profile of large endosomes containing extracellular debris and endosomes associated with primary lysosomal vesicles, which could support the notion that some of the pittings seen in the rounded Chang cells and the pathogenic amoebae are exit portals for endosome-lysosomes.