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C Garzelli

Publications and source records attributed to C Garzelli.

70 records · Page 4Linked 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

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

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↗
PubMed1978

An analysis of the role of lymphatic leukemia virus in the immunodepression exerted by Friend complex in leukaemia-resistant C57BL/6 mice.

Leukaemia-resistant C57BL/6 mice inoculated with the Friend complex (FLC) present a transient but definite depression of the ability to develop IgM and IgG antibody-producing cells to sheep red cells (SRC). In this paper it is shown that this immunodepression cannot be attributed solely to the lymphatic leukaemia virus (LLV) component of FLC which is immunodepressive in susceptible mice. This conclusion was reached by investigating the immunological reactivity of C57BL/6 mice following inoculation with two isolates of LLV. Circumstantial evidence obtained by examining the replication of FLC and LLV, the antibody response to E. coli lipopolysaccharide (LPS) and the ability of syngeneic macrophages administered together with the antigen to restore the response to SRC points to the same conclusion. There were also indications that the low sensitivity to depression by viruses of the Friend complex exhibited by the anti-LPS antibody response is due to the mitogenic activity of this antigen.

Animals↗
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↗
PubMedDate not supplied

Insulin-dependent diabetes: a possible viral disease.

The available information regarding the possible relevance of viruses in the pathogenesis of insulin-dependent diabetes is reviewed. Experimental studies in animals, clinical cases, histopathologic findings as well as epidemiologic and family studies provide circumstantial evidence that at least some cases of the disease are triggered by infection. Moreover, since it is widely accepted that autoimmunity plays a key role in diabetogenesis, the possible relationship between viruses and the induction of autoimmune responses to pancreatic islets is discussed. In view of recent developments in our comprehension of several chronic "idiopathic" diseases, the role of persistent viral infections and virus-induced immunopathology deserve further consideration in the etiology and pathogenesis of diabetes.

Animals↗
PubMedDate not supplied

Potential role of the Epstein-Barr virus in systemic lupus erythematosus autoimmunity.

OBJECTIVE: To investigate the possibility that Epstein-Barr virus (EBV), the agent of infectious mononucleosis (IM), may play a role in systemic lupus erythematosus (SLE). METHODS: EBV was searched for by PCR and by culture isolation in oropharyngeal lavage fluids of 15 SLE patients and, as controls, in 13 IM patients and in 28 healthy individuals with past EBV infection. Computer analysis was performed to select an antigenic domain of the virus-encoded nuclear antigen EBNA-2, in order to set up a synthetic peptide-based immunoassay. IgG antibodies to a 20-amino acid synthetic peptide derived from the selected domain of EBNA-2 (354GRGKGKSRDKQRKPGGPWRP373) were titrated in the sera of 20 SLE patients, 24 IM patients and 12 healthy subjects. RESULTS: EBV type 1 DNA was demonstrated by PCR in the oropharyngeal secretions of 8 SLE patients and the virus was isolated from 6 DNA-positive specimens. Moreover, 50% of the patients with SLE and 100% of the patients in the acute phase of IM, but none of the EBV-seropositive normal individuals, produced IgG antibodies to the EBNA-2-derived synthetic peptide. Computer analysis revealed a high degree of homology between the EBNA-2 354GRGKGKSRDKQRKPGGPWRP373 sub-sequence and the antigenic C-terminal domain 101GRGRGRGRGRGRGRGGPRR119 of the SmD1 ribonucleoprotein, a target of autoantibodies in a portion of SLE patients. CONCLUSION: We suggest the possibility that EBV may establish a persistent infection at least in a certain number of SLE patients. The antibodies elicited by the viral antigen EBNA-2 may cross-react with SmD1, thus indicating a role of EBV-specific immune responses in the outcome of SmD1 autoantibodies in SLE patients.

Antibodies, Viral↗