Changing concepts of infectious diarrheas.
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Biomedical subjects
Publications and source records attributed to S T Donta.
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Cell-free culture filtrates of heat-labile enterotoxin-producing strains of Escherichia coli are capable of inducing morphological changes and steroidogenesis in monolayer cultures of adrenal cells. These tissue culture changes are simiar to those induced by cholera enterotoxin and cannot be effected by culture filtrates of other enterotoxigenic or enteropathogenic types of bacteria. The results of the tissue culture studies correlated well with those done in the standard intestinal-loop systems and suggest that this tissue culture system could be used to significantly aid epidemiological and molecular studies with heat-labile Escherichia coli enterotoxin.
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Two clonal lines of rat hepatoma cells, in tissue culture, that have steroid-inducible tyrosine aminotransferase (TAT) activities were shown to have different responses to amphotericin B. One of the cell lines (HTC) was relatively resistant to the growth-inhibiting effects of amphotericin B and demonstrated an inhibition of only its steroid-inducible TAT activity when exposed to the antifungal agent. In contrast, not only was the other cell line (MHC) sensitive to amphotericin B during its growth, but uninduced and induced enzyme activities were affected. During the first few hours after the exposure of MHC cells to amphotericin B, both basal and dexamethasone-induced TAT activity were reduced; with continued exposure, enzyme activity increased over that of untreated cells and was superinduced in the presence of maximal, stimulating amounts of steroid. The mechanisms by which enzyme activity is induced by amphotericin B are probably different from those mediated by steroids.
Y1 adrenal cells in monolayer tissue culture react to culture filtrates from enterotoxigenic strains of Escherichia coli, but not to those from nontoxigenic strains, by undergoing morphological changes similar to those inducible by cholera enterotoxin and increasing their production of steroids. Heating destroys the ability of crude preparations of the E. coli enterotoxin to effect these tissue culture changes. None of a number of culture filtrates of other enteric or enteropathogenic bacteria were capable of inducing either the morphological changes or steroidogenesis. The maximal degree of steroidogenesis achievable with E. coli enterotoxin was comparable to that of cholera enterotoxin and could not be further increased by combination of the two toxins. As with cholera enterotoxin, removal of the E. coli toxin from the tissue culture medium after an initial brief exposure of the cells to the toxin was accompanied by some decrease in maximal steroidogenesis and no changes in either the onset or the permanency of the morphological changes. Antiserum raised to one of the crude E. coli enterotoxins was capable of completely neutralizing the steroidogenic effects and preventing the morphological changes secondary to a variety of different enterotoxigenic strains of E. coli. At the concentrations tested, this antiserum was not effective in preventing these same tissue culture changes inducible by cholera enterotoxin. The results of these and other related experiments suggest that cholera and heat-labile E. coli enterotoxins have similar mechanisms of action which are dissimilar to those of the other enterotoxins thus far described and tested.
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