Depression by
            <i>Pseudomonas aeruginosa</i>
            of Two T-Cell-Mediated Responses, Anti-
            <i>Listeria</i>
            Immunity and Delayed- Type Hypersensitivity to Sheep Erythrocytes

Petit, Jean‐Claude; Richard, G.; Albert, Beáta; Daguet, G

doi:10.1128/iai.35.3.900-908.1982

Cited by 25 publications

(21 citation statements)

References 15 publications

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“…Killed P. aeruginosa have also been demonstrated to inhibit cellular immunity to Listeria sp. and delayed hypersensitivity to sheep erythrocytes via a splenic, adherent, macrophage-like cell (22). In contrast, our results demonstrated a nonspecific, potent inhibition of lymphocyte DNA synthesis by high-dose P. aeruginosa.…”

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confidence: 78%

Suppression of in vitro lymphocyte DNA synthesis by killed Pseudomonas aeruginosa

et al. 1983

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Whole antibiotic-killed classic Pseudomonas aeruginosa organisms elicited human lymphocyte [3H]thymidine (TdR) uptake in vitro after 5 days in culture. However, high concentrations of the same preparation did not elicit [3H]TdR incorporation. The investigation of this lymphocyte unresponsiveness revealed that a high dose of P. aeruginosa, when added to lymphocyte cultures together with optimal concentrations of lymphocyte activators (e.g., plant lectins or whole killed Staphylococcus aureus Cowan 1), caused a potent, nonspecifically expressed inhibition of lymphocyte [3H]TdR uptake in response to these mitogens. High doses of P. aeruginosa were not cytotoxic to lymphocytes, and the inhibition caused was reversed when lymphocytes were washed free of bacteria. The inhibition of [3H]TdR uptake by high-dose P. aeruginosa did not require the generation of adherent suppressor cells or prostaglandin-mediated, steroid-sensitive or radiation-sensitive suppressor mechanisms. At optimal lymphocyte stimulatory concentrations of P. aeruginosa, the addition of indomethacin or the depletion of adherent cells caused an increase in lymphocyte [3H]TdR incorporation. This is consistent with an adherent-cell population regulating [3H]TdR uptake in response to P. aeruginosa via a prostaglandin-dependent pathway. This population was not involved in the inhibition of lymphocyte [3H]TdR uptake by high concentrations of P. aeruginosa.

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confidence: 78%

Suppression of in vitro lymphocyte DNA synthesis by killed Pseudomonas aeruginosa

et al. 1983

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“…A number of studies have shown that the opportunistic pathogen Pseudomonas aeruginosa can nonspecifically inhibit T-lymphocyte-mediated immunity in vitro (14,15,26,32,36) and in vivo (5,14,30). Patients infected with P. aeruginosa often show evidence of impaired cell-mediated immunity (28,33,34).…”

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confidence: 99%

“…In support of these clinical findings, Neely et al (25) demonstrated that infection with P. aeruginosa predisposed burned mice to lethal infections with Candida albicans. Two independent groups, Blackwood et al (5) and Petit et al (30), found that mice injected with P. aeruginosa were more susceptible to infection with the intracellular pathogen Listeria monocytogenes and showed a decrease in delayed-type hypersensitivity to Listeria and erythrocyte antigens.…”

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Inactivation of human gamma interferon by Pseudomonas aeruginosa proteases: elastase augments the effects of alkaline protease despite the presence of alpha 2-macroglobulin

et al. 1989

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Pseudomonas aeruginosa alkaline protease (AP) has recently been shown to produce limited proteolysis of human gamma interferon (IFN--y) and thereby destroy the antiviral and macrophage-activating activities of the lymphokine. In the present study we describe some of the characteristics of Pseudomonas elastase (E) with regard to inactivation of human IFN-,y. The inhibitory effect of E on IFN--y bioactivity differed from that of AP in that the direct effects of E were reduced in the presence of human serum. That this property of human serum was in large part attributable to the protease inhibitor a2-macroglobulin (%2-M) was suggested by the following observations: (i) methylamine treatment of serum reduced its effect on E, (ii) E interacted directly with OL2-M to induce a characteristic conformational change in the protease inhibitor, and (iii) preformed E-a2-M complexes lacked IFN-y-degrading activity. Despite these findings, anti-E antiserum partially neutralized the effect that a Pseudomonas filtrate showed on IFN--y, suggesting that E contributes to the activity of bacterial filtrates. Treatment of IFN--y with E in the presence of a suboptimal concentration of AP resulted in an E dose-dependent inactivation of the lymphokine. Preformed E-_2-M complexes, although ineffective by themselves at cleaving IFN-y, degraded the lymphokine, providing AP was also present in the reaction mixture.

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“…It has been previously reported that Pseudomonas aeruginosa decreases acquired cellular immunity to the facultative intracellular pathogen Listeria monocytogenes (27). P. aeruginosa injection results in the development of adherent, macrophage-like suppressor cells in the spleen and peritoneal cavity that are capable of preventing immunity of normal recipients against Listeria organisms.…”

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confidence: 99%

“…aeruginosa antigen. Antigen from P. aeruginosa was prepared as previously described (27) and consisted of the supernatant fluid of a heat-killed, 2-week-old, protein-free broth culture.…”

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confidence: 99%

Suppression of cellular immunity to Listeria monocytogenes by activated macrophages: mediation by prostaglandins

Petit¹,

Richard²,

Burghoffer³

et al. 1985

Infect Immun

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We previously demonstrated the suppression of cell-mediated immunity to Listeria monocytogenes by Pseudomonas aeruginosa-induced, macrophage-like cells. The present study was undertaken to evaluate the mechanism for this suppression. P. aeruginosa supernatant was shown to activate macrophages by the criteria of increased bactericidal capacities and increased attachment to glass surfaces. Acquired cellular resistance to L. monocytogenes could also be inhibited by macrophages from L. monocytogenes-pretreated mice. The depression of acquired immunity by P. aeruginosaor L. monocytogenes-activated macrophages did not appear to be due to a reduction of antigenic stimulus after nonspecific macrophage activation. In contrast, our findings suggest that suppression is mediated by activated macrophages through a prostaglandin-dependent mechanism. In vivo administration of aspirin blocked the immunosuppressive effect of P. aeruginosaor L. monocytogenes-activated cells. Moreover, the suppressive activity of supernatants of macrophages from Listeria-infected mice was reversed when indomethacin was present during supernatant generation. Finally, prostaglandin El treatment in vivo profoundly inhibited the induction of cell-mediated immunity to L. monocytogenes. The possible role and mechanism of prostaglandin in suppressing cellular immunity to intracellular bacteria are discussed. * Corresponding author. natants from these cells. Finally, our results demonstrated that prostaglandin E1 (PGE1) treatment in vivo profoundly disturbs the development of acquired immunity to L. monocytogenes. This study provides in vivo evidence that activated macrophages via arachidonic acid metabolites can suppress CMI to intracellular bacteria. MATERIALS AND METHODS Mice. Female Swiss CD-1 mice from Charles River Breeding Laboratories, Inc., Wilmington, Mass., were used

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Depression by Pseudomonas aeruginosa of Two T-Cell-Mediated Responses, Anti- Listeria Immunity and Delayed- Type Hypersensitivity to Sheep Erythrocytes

Cited by 25 publications

References 15 publications

Suppression of in vitro lymphocyte DNA synthesis by killed Pseudomonas aeruginosa

Suppression of in vitro lymphocyte DNA synthesis by killed Pseudomonas aeruginosa

Inactivation of human gamma interferon by Pseudomonas aeruginosa proteases: elastase augments the effects of alkaline protease despite the presence of alpha 2-macroglobulin

Suppression of cellular immunity to Listeria monocytogenes by activated macrophages: mediation by prostaglandins

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