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Biomedical subjects

M Campa

Publications and source records attributed to M Campa.

At least 73 records · Page 4Linked to original sources
PubMed1985

Polyclonal B cell activators inhibit contact sensitivity to oxazolone in mice by potentiating the production of anti-hapten antibodies that induce T suppressor lymphocytes acting through the release of soluble factors.

Polyclonal B cell activators (PBAs) such as purified protein derivative, lipopolysaccharide, Staphylococcus aureus strain Cowan I (StaCwI), and Pseudomonas aeruginosa inhibit contact sensitivity to oxazolone in mice when given 24 h before sensitization. This suppression, transferable from immunodepressed animals to oxazolone-sensitized recipients with immune serum, has been shown to be due to the early appearance of anti-hapten antibodies. These antibodies elicit T suppressor cells which release soluble factor(s) capable of inhibiting the passive transfer of contact sensitivity.

Animals↗
PubMed1984

T suppressor cells as well as anti-hapten and anti-idiotype B lymphocytes regulate contact sensitivity to oxazolone in mice injected with purified protein derivative from Mycobacterium tuberculosis.

Purified protein derivative from Mycobacterium tuberculosis inhibits contact sensitivity to oxazolone in mice when given intravenously 24 to 72 h before the antigen. Transfer experiments showed that various types of suppressor cells occurred in the lymph nodes draining the site of sensitization: (i) anti-oxazolone idiotype + B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients at the moment of their sensitization; (ii) anti-idiotype B lymphocytes, found at day 3 after sensitization, transferred suppression to syngeneic recipients when sensitization of these animals had been performed 3 days before cell transfer; (iii) T lymphocytes, found only at day 6 after sensitization, inhibited the passive transfer of contact sensitivity, indicating that they were effective on the efferent phase of the immune response. These results indicate that purified protein derivative from M. tuberculosis interferes with contact sensitivity by activating a complex and multiple immunoregulatory circuit.

Animals↗
PubMed1984

Staphylococcus aureus inhibits contact sensitivity to oxazolone by activating suppressor B cells in mice.

Killed Staphylococcus aureus strain Cowan I cells inhibit contact sensitivity to oxazolone in mice, when given intravenously 24-72 h before sensitization. With transfer experiments it was found that the cells responsible for the suppression are antigen-specific, nylon-adherent, resistant to antitheta serum + C, and sensitive to anti-mouse Ig serum + C. These suppressor B cells bear anti-oxazolone immunoglobulins and appear to exert their suppressive activity by preventing the contact sensitizer from reaching the specific reactive T cells.

Animals↗
PubMed1983

Auto-anti-idiotypic antibodies inhibit T-cell-mediated hypersensitivity in BCG-infected mice.

It is shown that serum from mice heavily infected with BCG contains antibodies which block the cell transfer of delayed-type hypersensitivity (DTH) to purified protein derivative (PPD) when BCG-immune cells were preincubated in it. This suppressive activity is antigen specific in that the serum does not block the cell transfer of contact sensitivity to oxazolone. However, the suppressive activity is not antigen directed in that it is absorbed neither by PPD-coupled Sepharose beads nor by PPD-pulsed normal peritoneal exudate cells. On the other hand, the activity can be absorbed to BCG-immune T cells and eluted from a Sepharose column conjugated with affinity-purified mouse anti-PPD antibodies. The possibility that antireceptor antibodies arise during the BCG infection and regulate DTH reaction is discussed.

Animals↗
PubMed1983

Regulation of the development of plaque-forming cells to bromelain-treated syngeneic mouse erythrocytes in bone marrow cell cultures.

The development of plaque-forming cells (PFC) to bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in bone marrow cell (BMC) cultures. It was found that the number of marrow PFC to Br-MRBC does not show the typical spontaneous increase observed in spleen cell (SPC), or peritoneal cell (PC) cultures. The number of anti-Br-MRBC PFC was markedly increased by lipopolysaccharide (LPS), even in conditions in which cell proliferation was blocked by mitomycin C, suggesting the presence of high numbers of Br-MRBC-specific precursor cells, potentially capable of differentiating into autoantibody-producing cells, in the marrow. Moreover, the low levels of anti-Br-MRBC PFC were further reduced in the presence of concanavalin A (Con A). The addition of Con A-activated BMC to BMC, SPC, or PC cultures actively suppressed the development of anti-Br-MRBC PFC. Con A-activated BM suppressor cells were found to be Thy 1.2-negative, Ig-negative, nonadherent cells. A possible role for the BM suppressor cell in tolerance to self antigens is discussed.

Animals↗
PubMed1983

Enhancement of the spontaneous development of autoreactive B cells by PPD in mouse peritoneal cell cultures.

The effect of tuberculin purified protein derivative (PPD) on the development of plaque-forming cells (PFC) against bromelain-treated syngeneic mouse red blood cells (Br-MRBC) was studied in peritoneal cell cultures. The finding that PPD enhances the development of PFC to Br-MRBC, even under conditions where cell division is blocked by mitomycin C treatment, suggests that cell proliferation does not represent a necessary prerequisite for differentiation of precursor cells into autoantibody-forming cells.

Animals↗
PubMed1983

Immunomodulation by Bacillus subtilis spores.

This study was undertaken in order to investigate the immunomodulatory effect of heat-killed Bacillus subtilis spores as well as of one soluble and one insoluble fraction obtained after their mechanical breakage. The results demonstrate that heat-killed spores, the soluble and the insoluble fraction enhance the primary PFC response to T-dependent antigens such as SRBC and HRBC, but not to T-independent antigens such as Ficoll-TNP. However, the same doses capable of enhancing the production of antibodies against T-dependent antigens were unable to modify the host CMI, evaluated in terms of contact sensitivity to oxazolone.

Animals↗
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

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↗