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R A FINKELSTEIN

Publications and source records attributed to R A FINKELSTEIN.

At least 19 recordsLinked to original sources
PubMed1964

ORIGIN AND PROPERTIES OF NATURALLY OCCURRING HAPTEN FROM ESCHERICHIA COLI.

Anacker, R. L. (National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratory, Hamilton, Mont.), R. A. Finkelstein, W. T. Haskins, M. Landy, K. C. Milner, E. Ribi, and P. W. Stashak. Origin and properties of naturally occurring hapten from Escherichia coli. J. Bacteriol. 88:1705-1720. 1964.-Haptens found in preparations of endotoxin and in fractions of disrupted cells, particularly one termed "native hapten," which appeared to be associated with the protoplasm of cells rather than with cell walls, have been further investigated with a view to establishing their origin and composition as well as their host-reactive properties. For this purpose, cells from a smooth strain of Escherichia coli O111:B4 were either extracted directly or disrupted and separated into cell-wall and protoplasmic fractions. Haptens were obtained by gel filtration of endotoxins, by trichloroacetic acid extraction of protoplasm, and by a mild acid hydrolysis of endotoxin. Several lines of evidence indicated that native hapten originated in the protoplasm rather than by autolysis or degradation of cell-wall endotoxin during procedures employed in disruption. In gel diffusion and quantitative precipitin tests, no hapten was identical with endotoxin, but native hapten was serologically the most complex of the haptens and precipitated the most antibody. Native and acid haptens, on a weight basis, fixed about 1% of the quantity of complement fixed by homologous endotoxin. Haptens did not stimulate the production of antibodies in mice or rabbits and did not elicit endotoxic host reactions. Chemically, native hapten differed from endotoxin and from acid hapten in that it lacked phosphorus, heptose, long-chain fatty acids, and 2-keto-3-deoxyoctonate. These substances did not appear to be determinants of antigenic specificity, but they may provide necessary bonds for assembling hapten-like units into fully antigenic and toxic macromolecules.

Animals↗
PubMed1960

Non-specific resistance to experimental cholera in embryonated eggs.

It has been confirmed that 11- and 13-day-old chick embryos are susceptible to lethal infection with minute inocula of V. cholerae, while 15-day-old embryos are relatively resistant. Twenty strains of E. coli were found to vary in their capacity to kill chick embryos, without relationship to their human enteropathogenicity. Prior infection of 13-day-old embryonated eggs with E. coli strains selected for low embryo virulence had a marked protective effect against superinfection with V. cholerae. This effect was duplicated by pretreatment of embryos with killed E. coli cells or endotoxin preparations but not with a suspension of killed cells of a Gram-positive species. Preparatory E. coli infection induces a phase of vibriostasis in the 13-day-old egg which may be sufficient to tide the embryo over into the phase of relative insusceptibility associated with age. Younger embryos exhibit only a lag in death under similar conditions. The chick embryo is presented as a potentially valuable tool for the study of combined infections and of the mechanisms of natural resistance.

Animals↗