Vibration of hamster small intestinal segments in hypotonic media containing PVP is a rapid method for obtaining quantitative yields of viable intestinal epithelial cells. This preparation of epithelial cells offers a unique system for the study of epithelial cell function in vitro. The method for cell separation combines hypoosmotic swelling of cells, which separates them at the desmosomes, with mechanical agitation which releases the cells from the lamina propria. No chemical agents known to affect cell proteins and cell surfaces are employed in this procedure. Only a short time is elapsed between in vivo and in vitro conditions, i.e., a preparation time of approximately 75 minutes. Although the technique yields a pure population of epithelial cells, the cells are of different morphologies, are removed from different areas of the crypts and villi, and therefore presumably have different functions. Examination of the intestinal tissue remaining after several vibration intervals by light and scanning electron microscopy indicates that the sequence of release of cells is removal of: (1) cells from the villus bases, (2) cells from the lower one-half to two-thirds of the villi, (3) cells from the villus tips (and some crypts), and (4) cells from the crypts. When pools of a+b cells are compared to pools of c+d cells, it is found that villus cells can be characterized by: (1) processes, such as monosaccharide absorption, associated with the brush border, and (2) synthesis of components (e.g., glycoproteins) of the brush border. Surprisingly, disaccharide hydrolytic activity is found in cells which transport monosaccharides poorly. The subpopulations of cells synthesize proteins equally.

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A major disease-inducing site for induction of experimental allergic encephalomyelitis in monkeys exists in Peptide P 14, the 37-residue segment of the Al protein comprising its COOH-terminus. The peptide appears to contain the dominant encephalitogenic determinant, since it was as active as the Al protein on a molar basis. By contrast, the 9-residue tryptophan region and the Peptide R region, active in guinea pigs and rabbits, respectively, were comparatively inactive in monkeys. The clinical and histologic expression of the disease produced by Peptide P 14 appeared identical to that induced by the intact Al protein.