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H H Freedman

Publications and source records attributed to H H Freedman.

17 recordsLinked to original sources
PubMed1973

Inhibition by oxisuran of cell-mediated hypersensitivity by decrease in numbers of specifically sensitized cells.

Oxisuran, 2-([methylsulfinyl]acetyl)pyridine, has previously been shown to selectively suppress cell-mediated immunity, as measured by prolongation of allograft survival, without inhibition of humoral immunity. In the present investigation, the influence of this compound on lymphoid cell transfer of delayed hypersensitivity was studied. In actively sensitized animals, including endotoxin-sensitized mice and rabbits, ovalbumin-, dinitrochlorobenzene-, and dinitrofluorobenzene-sensitive guinea pigs, or tuberculin-sensitive rats, daily treatment during the interval just preceding the elicitation and expression of the hypersensitivity was most inhibitory. In both endotoxin-sensitive mice and ovalbumin-sensitive guinea pigs, treatment of the sensitized cell donor just prior to lymphoid cell harvest and transfer resulted in inhibition of the expression of the hypersensitivity in untreated recipients. Approximately 10(4) fewer specifically sensitized lymphoid cells, but not fewer viable cells, were present in passively transferred cell preparations. In contrast, treatment of the lymphoid cell recipient in the same experimental model did not influence the expression of the transferred hypersensitivity. The results suggest that oxisuran may influence an as yet undefined event prior to the expression of a cell-mediated hypersensitivity response in sensitized animals.

Animals↗
PubMed1968

Induced sensitization of normal laboratory animals to Brucella abortus endotoxin.

A Boivin preparation of Brucella abortus, unlike common enterobacterial endotoxins, failed to depress water intake or increase numbers of hemolysin-producing spleen cells in mice, or to cause delayed inflammatory reactions in rabbit skin. Reactivity to the B. abortus endotoxin was found only in animals which were previously given the endotoxin with, but not necessarily in, complete Freund's adjuvant. Previous treatment with the endotoxin in saline or with only the adjuvant was ineffective. Sensitization appeared within 10 days and waned after 5 weeks. Passive sensitization was obtained with sensitized donor spleen cells but not with serum. Serum antibody titers did not correlate with the appearance and disappearance of sensitization.

Animals↗
PubMed1966

Relation of polysaccharide content to some biological properties of endotoxins from mutants of Salmonella typhimurium.

Kessel, R. W. I. (Rutgers, The State University, New Brunswick, N.J.), Henry H. Freedman, and Werner Braun. Relation of polysaccharide content to some biological properties of endotoxins from mutants of Salmonella typhimurium. J. Bacteriol. 92:592-596. 1966.-Endotoxins were extracted by the phenol-water procedure from a variety of Salmonella typhimurium mutants with known differences in the composition of their cell wall polysaccharides. The lethality of these preparations for mice proved to be correlated with the complexity of the polysaccharide: endotoxin from the smooth parent strain and from rough strains with several sugars attached to the heptose-phosphate backbone were of high toxicity, whereas endotoxin from a mutant possessing only glucose attached to the heptose-phosphate backbone was less toxic, and endotoxin from a mutant possessing the backbone only was least toxic. All of these mutants yielded endotoxins that were equally capable of protecting mice against subsequent challenge with Pseudomonas aeruginosa. Material obtained from a heptoseless mutant by the phenol-water method proved to be neither toxic nor protective. The apparent dissociation of biological properties that can be achieved with the aid of endotoxin preparations from certain mutants is discussed in terms of possible mechanisms.

Animals↗
PubMed1965

Endotoxin-induced susceptibility to staphylococcal infection and its reversal by adrenergic blocking agents.

Sultzer, Barnet M. (Princeton Laboratories, Inc., Princeton, N.J.), and Henry H. Freedman. Endotoxin-induced susceptibility to staphylococcal infection and its reversal by adrenergic blocking agents. J. Bacteriol. 90:1001-1006. 1965.-The transient phase of increased susceptibility to bacterial infection in mice provoked by prior administration of small doses of endotoxin was investigated for possible mediation by vasoactive substances. Animals were given endotoxin intravenously shortly before intraperitoneal injection of Staphylococcus aureus Smith, thereby lowering the lethal inoculum 10-fold. To determine whether this susceptibility state could be obviated, mice were pretreated with phenoxybenzamine or dibenzylchlorethylamine. Mortality decreased from an average of 81% in the endotoxin control groups to about 23% in the treated mice, closely approximating the mortality in control mice injected with saline and staphylococci. Neither antiadrenergic agent independently altered the resistance of mice to a higher lethal staphylococcal challenge, nor did these materials induce extravascular leukocyte mobilization into the peritoneal cavity. The results suggest a possible role of vasoactive staphylococcal alpha-toxin, as well as epinephrine or epinephrine-like factors, in this altered state of resistance to staphylococcal infection.

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