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B M Sultzer

Publications and source records attributed to B M Sultzer.

46 records · Page 3Linked to original sources
PubMed1975

Genetic control of B-cell responses. I. Selective unresponsiveness to lipopolysaccharide.

Spleen cells from C3H/HeJ mice fail to develop both proliferative responses and increased polyclonal antibody secretion in the presence of concentrations of the B-cell mitogen lipopolysaccharide that are optimal for the induction of B-cell responses in conventional strains. This unresponsiveness is selective for lipopolysaccharide, since C3H/HeJ spleen cells respond normally to two other polyclonal B-cell activators-dextran-sulphate and purified protein derivative of tuberculin. These findings are interpreted as indicating a selective defect in the B-cell subpopulation that responds to lipopolysaccharides in conventional strains.

Activation Analysis↗
PubMed1973

Purified protein derivative of tuberculin induces immunoglobulin production in normal mouse spleen cells.

Purified protein derivative (PPD) tuberculin induced immunoglobulin production in cultures of nonimmune mouse spleen cells, as measured by plaque-forming cells (PFC) against sheep erythrocytes (SRBC), horse erythrocytes, and 4-hydroxy-3,5-dinitrophenacetyl-SRBC. The increase started between 15 and 20 h of culture and reached a peak at 48-72 h. Higher PPD concentrations resulted in earlier peak responses than low concentrations. The Ig produced was mainly 19S and of very low avidity. The response elicited by PPD was of the same type as that caused by lipopolysaccharide of bacterial origin. Mitomycin treatment of cells before culture did not change the numbers of PFC/10(6) recovered cells but the cell recovery was considerably lower. Also injection of PPD in vivo resulted in increased numbers of PFC. On the basis of these results it is suggested that PPD nonspecifically activates a majority of the B cell population to proliferation and immunoglobulin synthesis.

Animals↗
PubMed1972

Genetic control of host responses to endotoxin.

Two pathophysiological effects of endotoxin in mice have been shown to be under the major influence of polygenic inheritance. The first, endotoxemia, was measured by LD(50) assays on hybrids and backcross hybrids of the resistant C(3)H/HeJ and the susceptible A/HJe strains. The LD(50) values of the F1 hybrids and the backcross hybrids were intermediate between the respective parental types. The second effect, the intraperitoneal extravascular leukocyte response to small doses of endotoxin, also was found to follow characteristic patterns of polygenic inheritance. As estimated from an analysis of the variance of mice of the F1 and F2 generations, the degree of genetic determination is approximately 54% for the neutrophil response and 82% for the monuclear response.

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.

Animals↗