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Biomedical subjects

H M Johnson

Publications and source records attributed to H M Johnson.

At least 199 records · Page 11Linked to original sources
PubMed1976

Interferon: effects on the immune response and the mechanism of activation of the cellular response.

The discovery of interferon in 1957 by Drs. Isaacs and Lindenmann led to major revisions in the concepts of man's defenses against viral infections. There are at least two types of interferon. Along with their antiviral properties, they have recently been shown to exert a suppressive effect on the humoral and cellular immune response; they affect both B and T lymphocytes. A variety of substances, including virus, polyribonucleotides, and mitogens for T lymphocytes, are good interferon inducers. T lymphocytes seem to be necessary for these inducers to exert their immunosuppressive effects. The immunosuppressive effects of interferon inducers suggests that interferons may be mediators of suppressor T lymphocyte effects. In the virus system, interferon does not exert its antiviral effects by direct action on the virus, but rather derepresses a cell gene that results in the production of an antiviral protein. This antiviral protein is probably the mediator of inhibition of virus replication. This is a complex sequence of events that results in the interaction of interferon with the cell membrane and the resulting production of the antiviral state in the cell. This review will examine the various steps of this involved process.

Animals↗
PubMed1975

Comparative inhibitory effects of antigen and antibody in the staphylococcal enterotoxin solid-phase radioimmunoassay system.

A solid-phase radioimmunoassay employing 125I-labeled enterotoxins and polystyrene tubes coated with specific antibody has been developed for assaying the relative concentrations of antibodies to staphylococcal enterotoxins A and B. Competitive binding occurs between tube-bound antibody and free antibody for binding sites on 125I-labeled enterotoxin. The sensitivity of the system is affected by the amount of antibody on the walls of the tubes, the concentration of 125I-labeled enterotoxin added to the system, and probably by the relative binding affinities of the bound and unbound antibodies. Antibody, 0.01 to 0.07 mug/ml, inhibited the uptake of 125I-labeled enterotoxin by 20%. Both the antibody and antigen solid-phase radioimmunoassay inhibition systems can be appropriately represented by either of the following two models: Loge (Y/1 - Y) = alpha0 + alpha1 LogeX and LogeY = beta0 + beta1 LogeX, where Y is bound activity, X is antigen or antibody concentration for inhibition, and alpha0, alpha1, beta0, and beta1 are regression coefficients. Estimates from the first model were slightly more precise for the antibody system, whereas the reverse was true for the antigen system.

Animals↗
PubMed1975

Stability of 125I-labeled staphylococcal enterotoxins in solid-phase radioimmunoassay.

Staphylococcal enterotoxins, Types A, B, and C, were labeled with 1252 by the chloramine-T method at approximately two levels of specific activity, 40 and 4 muCi/mug of protein. Toxins labeled with high specific activity showed extensive dissociation of 125I when stored at different temperatures, including -23 C. In contrast, toxins labeled with low specific activity did not show any significant loss of 125I when stored at -23 C for as long as 2 months. Enterotoxins, whether labeled with high or low activities, formed aggregates immediately upon labeling. Aggregate formation increased in high-activity-labeled toxins on storage at -23 C, and low-activity-labeled toxins showed no significant increase in aggregate formation, even after 2 months at -23 C. The aggregated forms of the enterotoxins were either devoid of antigenic activity in solid-phase radioimmunoassay or they possessed significantly reduced antigenic activity. Thus, a decrease in binding of 1252-labeled enterotoxin to specific antibody in solid-phase radioimmunoassay results mainly from (i) loss of 125I on storage, and (ii) formation of aggregates with reduced antigenic activity.

Binding Sites, Antibody↗
PubMed1975

Staphylococcal enterotoxin C: solid-phase radioimmunoassay.

A solid-phase radioimmunoassay test employing 125I-labeled enterotoxin C and polystyrene tubes coated with specific antibody was used for the detection and quantitation of entertoxin C in condensed milk, cheddar cheese, custard, and ham salad. The assay was sensitive to 1 to 10 ng of toxin per g of food; nonspecific inhibitions were 16% or less.

Enterotoxins↗
PubMed1975

Inhibitory effect of synthetic polyribonucleotides on the primary in vitro immune response.

The synthetic double-stranded polyribonucleotides, poly (rA):poly (rU) and poly (rI):poly (rC), were shown to be potent inhibitors of the in vitro plaque-forming cell (PFC) response to a thymus-dependent (SRBC) and thymus-independent (E. coli 0127 LPS) antigen in mouse C57BL/6 spleen cell cultures. The same polynucleotides had no effect on the PFC response of nude (athymic) mouse spleen cells to E. coli 0127 LPS, suggesting that functional T lymphocytes are necessary for the inhibitory effect. Enhancement effects were modest and inconsistent in the cultures. Poly (rA) and poly (rU) were ineffective as inhibitors. The data indirectly suggest that the inhibition may be due to the early production of interferon by functional T lymphocytes.

Animals↗
PubMed1975

Tartrazine: solid-phase radioimmunoassay studies of an azo dye implicated in allergic reactions (azo dyes and allergy).

A solid-phase radioimmunoassay procedure was adapted for the haptenic study of tartrazine, an azo dye implicated in various forms of allergy. Further, the haptenic relationship of tartrazine and aspirin was investigated, since sensitivity of individuals to the two substances is often clinically associated. The specificity of antibody to tartrazine was directed strongly toward a pyrazolone intermediate of the molecule, 1-(4-sulfophenyl)-3-carboxy-5-hydroxy-pyrazole. Aspirin did not cross-react with anti-tartrazine, suggesting that the clinical association of aspirin and tartrazine sensitivity in patients is a nonimmunological phenomenon.

Antigens↗
PubMed1975

Inhibition of the primary in vitro antibody response by interferon preparations.

The primary in vitro plaque forming cell (PFC) response of mouse (C57BL/6J) spleen cells to sheep red blood cells (SRBC) was inhibited by two sources of crude and two sources of partially purified mouse interferon. The substance(s) in the interferon preparations which induced PFC and antiviral inhibitory activity have the following common characteristics: a) The interferon preparations were of different potencies and specific activities, but they inhibited the PFC response in proportion to their activities; 20 to 60 units were the minimal amounts required for greater than 90% inhibition of the PFC response. b) Both the antiviral activity and the PFC inhibitory activity of the interferons were neutralized by antibody specific for mouse interferon. c) Both activities were partially or completely inactivated by heating at 60 degrees C for 1 h. d) Human interferons had neither antiviral activity nor PFC inhibitory activity in mouse cells. e) Limited exposure (4 h) of cells to interferon significantly inhibits both viral infection and the PFC response. f) Both the antiviral activity and the PFC inhibitory activity of the interferon preparations are acid stable. It is concluded, therefore, that the inhibition of the primary in vitro PFC response is due to interferon in the preparations. Maximum inhibition of the PFC response occurred when interferon was added to cultured at the same time as SRBC. Significant inhibition was also observed when interferon was added 1 day later, and slight enhancement was observed when added at days 2 and 3 of SRBC addition. Kinetic data showed that the greater the concentration of interferon added to the cultures, the earlier the effect on the PFC response. The presence of interferon in cultures for the first 4 h is sufficient to inhibit the PFC response. Interferon, then, appears to affect some early event(s), which leads to inhibition of the PFC response. Since mature T cells can be one of the sources of interferon, we have demonstrated a suppressor effect of a T cell lymphokine. The precise relationship of interferon to various expressions of suppressor T cell effects remains to be determined.

Animals↗
PubMed1975

The effect of staphylococcal enterotoxins on the primary in vitro immune response.

Staphylococcal enterotoxins, like several plant lectins, have been shown to stimulate mitogenic activity and lymphokine production in lymphocytes. The effect of enterotoxins A and B on the primary in vitro plaque-forming cell (PFC) response of mouse (C57BL/6) spleen cells to sheep red blood cells (SRBC) was examined. PFC responses in 4- or 5-day cultures were inhibited greater than 90% by 0.1 mug enterotoxin A and by 3- to 6-mug enterotoxin B when the toxins were added to the cultures either at the time of SRBC addition or 24 hr before. Both enterotoxins A and B were shown to be T lymphocyte mitogens. Kinetic data indicated that the enterotoxins (10 mug) inhibited the PFC response as early as day 3, but were relatively more inhibitory at days 4 and 5. The PFC response was inhibited when enterotoxins were added to cultures at the same time as antigen or a day later; it was enhanced when added at day 2; and it was unaffected when added at day 3 of 4-day cultures. Further, the presence of enterotoxin A during the first 24 hr of culture and subsequent removal was still as effective in inhibiting the PFC response as when it was present throughout the culture period. The PFC inhibitory properties of enterotoxins appear, then, to affect some early event(s) in the in vitro immune response. Alpha-methyl-D-mannopyranoside blocked the PFC inhibitory effect of concanavalin A (con A), but it had no effect on enterotoxin A. The two mitogens appear, then, to react with different receptors on the lymphocytes or to differ in the dynamics of their reactivity. The effects of staphylococcal enterotoxins on the PFC response of spleen cells were remarkably similar to those reported for lectins such as con A. Enterotoxins are structurally simpler than con A and should therefore be quite useful in studying various biologic activities of lymphocytes.

Animals↗
PubMed1973

Respiration-independent Binding of SR to Bean Mitochondria.

Binding of Sr(2+) to bean mitochondria (Phaseolus vulgaris) shows a dissociation constant of 25 x 10(-6) and results in 40 to 50 nmoles of Sr(2+) bound per mg protein. The binding is partially inhibited by valinomycin plus K(+), 2, 4-dinitrophenol, as well as ruthenium red at a level of the 120 nmoles per mg protein. These compounds also partially inhibit active uptake of Sr(2+). Calcium and Mg(2+) also partially inhibit binding in the same magnitude as previously reported for inhibition of transport. Phosphate which is required for divalent cation transport is without effect on the binding of Sr(2+). The possible role of the observed binding sites in divalent cation transport is discussed.

Journal Article↗
PubMed1973

Staphylococcal enterotoxins A and B: solid-phase radioimmunoassay in food.

An immunoassay employing (125)I labeled enterotoxins A and B and polystyrene tubes coated with specific antibodies was used for detection and quantitation of enterotoxin in food. Ham salad, cheddar cheese, custard, condensed milk, and salami were studied. Enterotoxin was successfully determined in all the foods by simple extraction procedures. The assay was sensitive to 1 to 10 ng of toxin per g of food; nonspecific inhibitions were 15% or less.

Animals↗