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Biomedical subjects

G Falcone

Publications and source records attributed to G Falcone.

At least 109 records · Page 6Linked to original sources
PubMed1982

Impairment of cell-mediated immunity in Pseudomonas aeruginosa pyelonephritis: lack of suppressor cell activity in vivo.

Bacterial pyelonephritis was induced in mice by direct microinoculation of Pseudomonas aeruginosa in the kidney. In the acute phase of P. aeruginosa pyelonephritis, a state of cell-mediated immunity impairment, evaluated both in vitro as lymphocyte reactivity to concanavalin A and in vivo as host versus graft reaction has been observed. Furthermore, delayed-type hypersensitivity to specific bacterial antigen has been detected only when the kidney infection was subsiding, i.e., 3 weeks after bacteria inoculation. When investigating the mechanism of such T-cell impairment, we were unable to transfer the immunodepression, suggesting that suppressor cells are not involved in vivo. The role of P. aeruginosa inhibition of cell-mediated immunity in the pyelonephritic host is discussed.

Animals↗
PubMed1982

Cell-mediated immunity and delayed-type hypersensitivity in Pseudomonas aeruginosa-infected mice.

In mice repeated systemic injections of Pseudomonas aeruginosa viable cells were able to induce a specific delayed-type hypersensitivity, which was evaluated as increase both in footpad swelling and in the weight of popliteal lymph nodes, after a challenge in the footpad. Unfractionated spleen cells or T lymphocyte-enriched spleen cells from sensitized donors were able to specifically transfer the delayed-type hypersensitivity to syngeneic recipients but failed to protect them against a lethal challenge with P. aeruginosa. In contrast, serum or B lymphocyte and macrophage-enriched spleen cells from the same donors were capable of transferring protective immunity but failed to induce any delayed-type hypersensitivity reaction in the recipients. These results clearly show that in systemic P. aeruginosa infections a dissociation between delayed-type hypersensitivity and acquired cellular resistance occurs.

Animals↗
PubMed1982

The suppressive activity of T-lymphocytes and serum factors in burned patients.

This study was performed to investigate the cell-mediated immune response in burned patients with no septic episodes. The results show that burned patients with percentage body burn higher than 20 had an impaired lymphocyte reactivity to phytohaemagglutinin and conconavalin A. This hyporesponsiveness appeared on day 3-4 and in all cases reached its maximum on day 7-8 post burn, while recovery occurred between day 11 and 29 depending on the severity of the injury. The serum from immunodepressed patients was able to inhibit the response to phytohaemagglutinin and conconavalin A of normal lymphocytes. This immunosuppressive activity was present very early after injury (on day 1-2) and before the onset of lymphocyte hyporesponsiveness to mitogens and was no longer detectable on day 7-8 post burn, when patient lymphocytes showed the greatest hyporesponsiveness to mitogens. This late depression was due to T suppressor cells.

Adolescent↗
PubMed1982

Evidence for autoantibody production associated with polyclonal B-cell activation by Pseudomonas aeruginosa.

Experimental infection of mice with Pseudomonas aeruginosa resulted in the polyclonal activation of B lymphocytes, as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and sheep erythrocytes. Additionally, a PFC response to bromelain-treated syngeneic erythrocytes (Br-MRBC) could be detected in infected mice, suggesting that P. aeruginosa infection might also induce activation of self-reactive B-cell clones and consequently lead to autoantibody production. Furthermore, in cultures of mouse peritoneal cells, heat-killed P. aeruginosa enhanced the development of anti-Br-MRBC PFC, even under conditions where cell division was blocked, suggesting that the in vitro P. aeruginosa-induced enhancement of anti-Br-MRBC PFC was essentially related to cell differentiation, cell division playing only a minor role. The mechanism of the in vivo and in vitro P. aeruginosa-induced activation of anti-Br-MRBC PFC are discussed.

Animals↗
PubMed1982

Urinary excretion of oxalate in renal failure.

The daily urinary excretion of oxalate has been found to be lower than normal in patients with renal failure and the decrease to be directly proportional to the impairment of renal function. It has also been found that the gut flora from uremic patients destroys oxalate 'in vitro' more efficiently than the gut flora from normal people. It is postulated that an adaptation occurs in the gut flora of uremics to 'metabolize' oxalate, and this enteric elimination may account for its decreased urinary excretion.

Humans↗
PubMed1982

LPS-induced enhancement of plaque-forming cell response to bromelain-treated syngeneic erythrocytes in mouse peritoneal cell cultures.

The effect of bacterial lipopolysaccharide (LPS) on the development of plaque-forming cells (PFC) against bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in peritoneal cell (PC) cultures. It was found that LPS enhances the development of PFC to Br-MRBC and increases DNA synthesis in PC cultures. The LPS-induced enhancement of PFC to Br-MRBC, however, does not appear to require cell proliferation, since it also occurred in PC cultures pretreated with mitomycin C. In addition, the LPS-induced B lymphocytes blastogenesis is under the control of macrophages, while cell differentiation of precursor B lymphocytes into cells actively producing antibodies against Br-MRBC is regulated by suppressor T lymphocytes.

Animals↗
PubMed1982

Role of specific delayed-type hypersensitivity in Pseudomonas aeruginosa-infected mice.

The role of specific cell-mediated immunity was studied in mice injected in the hind footpad with viable Pseudomonas aeruginosa cells. The results reported here show that a state of specific delayed-type hypersensitivity, evaluated both as footpad swelling and as weight increase of popliteal lymph node, occurs in P. aeruginosa-infected mice. Furthermore, a T-cell-enriched spleen population from infected animals was able to transfer delayed hypersensitivity to normal recipients. However, identity at the major histocompatibility complex to transfer delayed hypersensitivity was required. Acquired cellular resistance was not transferred to normal recipients by immune T lymphocytes. On the contrary, mice receiving immune T cells showed an increase in the severity of the lesion caused by a viable challenge. The dichotomy between acquired cellular resistance and delayed hypersensitivity, and the possibility that T-cell reactivity to P. aeruginosa may be actively controlled, is discussed.

Animals↗
PubMed1980

Mouse footpad infection by Pseudomonas aeruginosa: evidence for delayed hypersensitivity to specific bacterial antigen.

Mouse hind footpad inoculation with 1 x 10(7) viable Pseudomonas aeruginosa cells produces a long-lasting, self-limiting disease process characterized by a bacterial multiplication that parallels the swelling of the infected footpad. Regional popliteal and inguinal lymph nodes and spleen of infected animals show cellular modifications which are almost entirely due to lymphocyte proliferation, as indicated by sponteneous DNA synthesis experiments in vitro. Furthermore, mice which had been infected in their footpad either 20 or 27 days previously and challenged with P. aeruginosa antigens into the controlateral footpad show, 24 h later, a marked increase in regional popliteal lymph node weight, indicating the development of delayed hypersensitivity to Pseudomonas antigens.

Animals↗
PubMed1979

Pseudomonas aeruginosa infection depresses contact sensitivity to oxazolone by enhancing suppressor cell activity.

The depression of contact sensitivity to oxazolone in mice infected with Pseudomonas aeruginosa was studied. In oxazolone-sensitized mice, P. aeruginosa infection affects cell proliferation in the lymph nodes draining the site of sensitization. This impaired cell proliferation does not seem to be due to an altered lymphocyte reactivity, since lymph node and spleen cells from infected animals show a normal mitotic responsiveness to both T and B cell mitogens. In addition, the draining lymph nodes and spleens of mice exhibiting a depressed response to oxazolone contain a cell population able actively to suppress the response to the same antigen of syngeneic recipients sensitized immediately before the cell transfer. These suppressor cells require antigenic stimulation and appear to act on the induction phase of contact sensitivity.

Animals↗
PubMed1979

Depression of the antibody response in Pseudomonas aeruginosa-injected mice.

Heat-killed Pseudomonas aeruginosa inhibit antibody response in C57BL/6 mice. The depression of this response is dependent on the dose of bacteria injected, on the time interval between microorganism injection and antigen administration, and on the nature of the antigen used. Cell transfer experiments provide evidence that suppressor cells are not operative in this model. Furthermore, the results show that P. aeruginosa induces a marked dose-dependent proliferation of spleen cells in vivo, and the in vitro targets of this proliferative effect are B lymphocytes. It is suggested that whole, heat-killed P. aeruginosa in vivo also behave as cell mitogens on B lymphocytes which, when strongly stimulated to proliferate, temporarily lose their capacity to mount a normal antibody response.

Animals↗
PubMed1979

Depression of contact sensitivity by Pseudomonas aeruginosa-induced suppressor cells which affect the induction phase of immune response.

The cellular basis of depression of contact sensitivity to oxazolone in mice injected with Pseudomonas aeruginosa was studied. Cells from draining lymph nodes of mice sensitized with oxazolone 18 h previously were able to induce contact sensitivity to normal mice when administered in their footpads. In contrast, cells from draining lymph nodes of P. aeruginosa-injected and oxazolone-sensitized donors failed to induce contact sensitivity when injected in the footpad of normal mice and were capable of actively blocking the immunizing process brought about by lymph node cells from sensitized mice when injected together in the footpad of normal recipients. The P. aeruginosa-induced suppressor cells required antigenic stimulation, had precursors sensitive to cyclophosphamide, and did not affect the effector mechanisms of contact sensitivity. Thus, the results suggest that P. aeurginosa depresses contact sensitivity to oxazolone by enhancing the activity of suppressor cells which normally arise during the sensitization process and which affect the afferent limb of the immune response, probably by inhibiting the normal recruitment of T lymphocytes in the draining lymph nodes.

Animals↗