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Biomedical subjects

G Falcone

Publications and source records attributed to G Falcone.

At least 127 records · Page 7Linked to original sources
PubMed1978

Depression of contact sensitivity by enhancement of suppressor cell activity in Pseudomonas aeruginosa-injected mice.

Heat-killed Pseudomonas aeruginosa depresses contact sensitivity to oxazolone in C56BL/6 mice. The draining lymph nodes and spleens of mice exhibiting an impaired reactivity to oxazolone contain a cell population capable of depressing the response to oxazolone of recipients sensitized immediately before cell transfer. The suppressive activity of these cells appears to be antigen specific, since they do not affect the response to picryl chloride and because they do not arise in P. aeruginosa-injected but not oxazolone-sensitized mice. These suppressor cells occur in the draining lymph nodes and spleen at 3 and 4 days after sensitization, respectively, and have precursors sensitive to cyclophosphamide. It is concluded that P. aeruginosa depresses contact sensitivity to oxazolone by enhancing the suppressor cell activity of the regulatory cells which arise during conventional sensitization.

Animals↗
PubMed1976

Evidence for suppressor cell activity associated with depression of contact sensitivity in Pseudomonas aeruginosa infected mice.

Pseudomonas aeruginosa infection depresses contact sensitivity to 2-phenyl-4-ethoximethylene-oxazolone (oxazolone), and enhances the antibody response to sheep erythrocytes (SRBC) in the mouse. Anti-oxazolone antibody titres were found not to be significantly different in infected and uninfected animals; thus, the major circulating classes of antibodies do not seem to be responsibile for the observed depression of skin reactivity. Low dose (20 mg/Kg) cyclophosphamide (CY) pretreatment induced a further potentiation of antibody response to SRBC, and prevented depression of contact sensitivity in infected mice. On the other hand, when infected animals were pretreated with high doses (200 mg/Kg) of CY, antibody production was completely suppressed, whereas contact sensitivity was unaffected. Since CY treatment is known to selectively inhibit B lymphocytes, and since it can abrogate the infection-induced depression of reactivity to oxazolone, it is suggested that suppressor cells, which may have B-cell characteristics, are stimulated during P. aeruginosa infection in the mouse.

Animals↗
PubMed1975

Depression of contact sensitivity and enhancement of antibody response in Pseudomonas aeruginosa-infected mice.

The effect of Pseudomonas aeruginosa infection on contact sensitivity to 2-phenyl-4-ethoximethylene-oxazolone (oxazolone) and on antibody response to sheep erythrocytes, horse erythrocytes, and Escherichia coli 0111:B4 lipopolysacharide was investigated in outbred C57BL/6 mice. Injection of 0.5 and 0.2 median lethal doses significantly depressed contact sensitivity to oxazolone, whereas injection of 0.5 median lethal dose of heat-killed microorganisms did not. The filtrate of a 24-h broth culture did not affect contact sensitivity as well. Antibody production against sheep erythrocytes, horse erythrocytes, and lipopolysaccharide (evaluated as plaque-forming cells and circulating hemagglutinin and hemolysin titers) was found to be significantly enhanced both in animals injected with living bacteria and in those which received heat-killed microorganisms. The simultaneous occurrence of depression of cell-mediated immunity and potentiation of humoral response suggests that P. aeruginosa might interfere at different levels of the host immunological responsiveness.

Animals↗
PubMed1975

Regulation of breakdown and synthesis of L-glutamate decarboxylase in Clostridium perfringens.

L-Glutamate decarboxylase (GAD) activity of Clostridium perfringens (ATCC 8009) cells grown in various culture conditions was investigated. Remarkable variations of GAD level occur during the growth cycle in thioglycollate broth. These changes are affected by the pH of the culture medium. Addition of alkali to the culture media results in decrease of cell GAD activity, whereas increase of enzyme level occurs only in cells growing in unbuffered media. The results indicate that the mechanism regulating the GAD levels is sensitive to the changes of pH (or buffering substances) rather than to the steady pH values. Neither repression by glucose nor induction by L-glutamate was observed. Moreover, high concentrations of the free amino acid substrate in the culture media considerably decrease cell GAD activity, owing to the buffering effect of the amino acid. The molecular mechanism supporting the variations of GAD activity during the growth cycle of the cells were investigated and tentatively related to the structural and functional properties of the pure enzyme. It is shown that the drop of GAD activity during the lag phase is due to protein breakdown. Evidence is presented suggesting a control of protein degradation by its quaternary structure. Data are also reported supporting de novo synthesis of GAD during the late logarithmic phase of cell growth. Finally, the possible role of GAD as part of the pH regulation system of C. perfringens cells is discussed in relation both to physiologic conditions of the bacterial cell and to the molecular mechanisms regulating the GAD activity in vivo.

Carboxy-Lyases↗