Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human gingival fibroblasts were exposed in culture to cell extracts of different black-pigmented Bacteroides species, and their growth was monitored by determining thymidine uptake and counting cells. Of the Bacteroides species tested (B. gingivalis, B. asaccharolyticus, and B. intermedius), B. gingivalis gave the extract with the strongest inhibitory effect on fibroblast thymidine uptake. Linear inhibition reaching 80% of the control level was obtained with a dose of 100 micrograms of B. gingivalis extract protein per ml. The effect of B. asaccharolyticus resembled that of B. gingivalis, but even at the highest dose tested B. intermedius had only a slight inhibitory effect. When fibroblasts were counted after 2- and 4-day exposures to B. gingivalis extracts, a clear depression in the number of fibroblasts was found. The effects of extracts obtained from early and late growth phases of B. gingivalis cultures were similar. A fraction of B. gingivalis consisting essentially of lipopolysaccharides (LPSs) was obtained by degrading the extract proteins with proteinase K. Silver staining of polyacrylamide gels revealed a LPS pattern with a molecular mass ranging from 37 to 60 kilodaltons. This LPS-rich fraction caused inhibition of thymidine uptake by gingival fibroblasts similar to that caused by the native extract alone. Thus, the inhibition of gingival fibroblast growth by B. gingivalis appeared to be LPS mediated. This inhibitory effect of B. gingivalis on oral fibroblast growth may be a virulence factor of this bacterium.
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PMID:Inhibition of gingival fibroblast growth by Bacteroides gingivalis. 379 30

Sinomenine, an epimorphinan alkaloid, was tested for the immunosuppressive effect in mice. This compound produced a decrease of plaque-forming cells (PFC) to a T cell-dependent antigen, sheep red blood cells, in vivo. The depression of the PFC response induced with sinomenine was dose and time dependent. On the other hand, it failed to suppress the PFC response to a T cell-independent antigen, lipopolysaccharide. The immunosuppressive dose of sinomenine did not alter the cellularity of spleen, thymus, bone marrow and peripheral blood leucocytes, the DNA synthesis activity of bone marrow cells nor the proliferative responses of spleen cells induced by T cell and B cell mitogens in unprimed mice. These data suggest a selective effect of sinomenine on lymphoid cells. This compound has a potential for use in studies of immuno-deficiencies or clarifying some aspect of immunity.
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PMID:Effect of sinomenine on antibody responses in mice. 387 42

The effects of carbon dust inhalation on the bone marrow-derived (B) and thymus-derived (T) lymphocyte populations of spleen and mediastinal lymph node (MLN) cultures were examined. The concanavalin A (Con A)-responsive cell population (T cells) in the spleen was found to be depressed after 7 days of pre-exposure to carbon dust. However, this effect was transient, and after 14, 21, and 28 days of pre-exposure to carbon dust, the Con A-responsive cells exhibited a 30 to 40% enhancement over control group responses. Conversely, Con A-responsive cells in the pooled MLN cultures exhibited depression, ranging from 22 to 33% below control group values, after 7, 14, and 28 days of pre-exposure to carbon dust. The lipopolysaccharide (LPS)-responsive cell population (B cells) in the spleens of carbon-exposed mice was found not to differ significantly from control group values after all times of pre-exposure. LPS-responsive cells in the MLN cultures exhibited enhancement, ranging from 49 to 74% above control values, after 14, 21, and 28 days of pre-exposure to carbon dust. The ability of carbon spleen cell cultures from carbon-exposed mice to undergo antigen induced blast transformation after sensitization with Mycobacterium tuberculosis H37Ra was also determined. Mice exposed to carbon dust inhalation 2 weeks before and 3 weeks after aerosol or subcutaneous immunization exhibited significantly enhanced ratios of transformation upon culture of their spleen lymphocytes with purified protein derivative of tuberculin.
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PMID:Effects of carbon dust inhalation on the cell-mediated immune response in mice. 420 26

The nonspecific functional capacity of spleen cells, taken from female guinea pigs with primary acute cytomegalovirus (CMV) infection, was assessed using lipopolysaccharide (LPS), a B-cell mitogen, and concanavalin A (Con A), a T-cell mitogen. Proliferative responses to the two mitogens were found to be significantly depressed in animals inoculated with CMV as compared to control animals. The defect in Con A responsiveness occurred earlier during the course of the infection than the defect in LPS responses. Although responses to the mitogens were depressed at the time of peak virus activity in the spleen, the possibility of lytic destruction of the spleen cells by the virus during in vitro culture was excluded. In addition, the depression in Con A responsiveness was noted with a wide range of Con A concentrations, and preculture studies failed to result in enhanced reactivity of the cells from infected animals. We conclude that reductions of both B- and T-cell functions, which differ in their timing during the course of acute CMV infection, occur concurrently with an enhanced viral specific immune response in guinea pigs acutely infected with CMV.
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PMID:Asynchronous depression of responses to T- and B-cell mitogens during acute infection with cytomegalovirus in the guinea pig. 608 91

The primary antibody response of BALB/c splenocytes to sheep erythrocytes in vitro was suppressed by infection with Friend leukemia virus (FLV), with the response capacity decreasing with increasing duration of infection. The acquisition of normal antibody responses was amplified by macrophage-produced antibody response helper factor(s). FLV-infected mice were treated with bacterial lipopolysaccharide to induce the release of these helper factors into the serum. Similar to the loss of antibody response capacity by their splenocytes, the FLV-infected mice progressively lost the ability to produce helper factors in response to lipopolysaccharide. In vitro cultures of FLV-infected cells also showed a depressed ability to produce helper factor activity both spontaneously and in response to lipopolysaccharide stimulation. The reconstitution of normal levels of exogenous helper factors to FLV-infected splenocytes restored the antibody response to normal or even elevated levels. These studies indicate that the mechanism for suppression of antibody responses by FLV involves the depression of antibody response helper factor production.
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PMID:Role of antibody response helper factors in immunosuppressive effects of friend leukemia virus. 622 Sep 70

The effect of the nonsteroidal estrogenic compound, diethylstilbestrol (DES) on cell-mediated immunocompetence in the mouse has been assessed. Adult female B6C3F1 mice were injected (s.c.) with 0.2, 1.0 and 4.0 mg/kg of DES daily for 14 days. All immunological tests and toxicological parameters were determined at least 24 hr after the last exposure. Thymic involution and hepatomegaly were noted at the lowest dose of DES. The most sensitive indicator of immunosuppression by DES was the delayed hypersensitivity response (DHR) to keyhole limpet hemocyanin in mice sensitized without adjuvant. The lowest dose of DES produced a 93% decrease, compared with a 39% decrease for the same DHR model in mice sensitized to keyhole limpet hemocyanin plus adjuvant and a 63% decrease for the DHR to sheep erythrocytes. A 35% decrease of the acute inflammatory response to carrageenin was produced by the lowest dose of DES. Day 2 proliferative responses to both concanavalin A and phytohemagglutinin (T-cell mitogens) were depressed by the lowest dose of DES, whereas significant suppression of the response to lipopolysaccharide (B-cell mitogen) was only noted at the highest dose of DES. The effects of DES on Day 3 proliferative responses were less dramatic. The mixed lymphocyte response was significantly suppressed by 1.0 and 4.0 mg/kg of DES on all days in culture. The reversibility of the DES effects was studied by resting the mice for 30 days between exposure and measuring a given parameter. All effects on organ weights and the depression of both the sheep erythrocytes DHR and the carrageenin inflammatory response were reversed.
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PMID:Suppression of cell-mediated immunocompetence after subchronic exposure to diethylstilbestrol in female B6C3F1 mice. 622 65

Recent studies have provided evidence that deficient interleukin-2 (IL-2) production by helper T cells contributes to the impaired T-cell-mediated functions observed in aged mice. Since most of these responses depend upon the presence of macrophages, a deficit in the functional capacity or in cell cooperation of macrophages may result in a decrease in immune reactivity. We found in the present study, that in vitro the cytostatic activity of macrophages from aged C57BL/6 (B6) mice is affected only slightly, but that in vivo their number increases with age. The synthesis of IL-1 is reduced when macrophages from aged mice are stimulated in vitro by lipopolysaccharide, but addition of exogenous IL-1 apparently does not restore either the mixed lymphocyte reaction or cytotoxic T lymphocyte generation. Co-cultures of young splenic macrophages with aged T lymphocytes do not restore to normal level the impaired proliferative response to T mitogens of aged B6 mice, but aged splenic macrophages provide a full accessory help for mitogenesis of young T cells. Thus, absorption of IL-1 by phytohemagglutinin-activated T cells is slightly altered in aged mice. IL-2 responsive T cells are not altered since exogenous IL-2 supply in vitro completely reconstitutes cytotoxic T lymphocyte generation after an allogeneic stimulation. Moreover, the number of Lyt 1+ cells is not modified in aged B6 mice. These results suggest that the impaired capacity of macrophages to release IL-1 and of blast T cells to bind IL-1 may contribute to the depression of cell-mediated immune reactivity associated with aging but also that the main defect is a functional lesion of IL-2 production by Lyt 1+ helper T cells.
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PMID:Interleukin-1 synthesis and activity in aged mice. 623 33

Comparative studies on tumor and adjuvant-induced depression of in vitro mitogen responses were carried out using spleen cells obtained from syngeneic tumor bearing (TB) ACI rats or from rats which had been immunized with BCG cell walls attached to oil droplets (BCGcw). These in vitro studies demonstrated that: 1) the spleen cells from TB rats (TB-spleen cells) showed strongly depressed mitogen responses to concanavalin-A (Con-A), phytohemagglutinin-P (PHA-P) and lipopolysaccharide (LPS), 2) the mitogen response of lymph node cells from TB rats was slightly depressed, 3) the removal of plastic or nylon-wool adherent cells or phagocytic cells from TB-spleen cells resulted in a restoration of the mitogen response, 4) the Con-A response of normal spleen cells could be suppressed by the addition of TB-whole spleen cells, 5) the suppressor cell activity was not abrogated by the in vitro treatment with x-irradiation (2000 rads), 6) carbonyl-iron treated TB-spleen cells showed a normal level of mitogen response, and on addback to normal spleen cells no suppressive activity was detected in them. Similar results were observed when spleen cells were obtained from BCGcw immunized rats. These results suggest that in ACI rats tumor-induced nonspecific suppressor cells detected by in vitro assay are the same cell populations as BCGcw-induced nonspecific suppressor cells.
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PMID:Comparative studies on tumor and adjuvant (BCGcw)-induced nonspecific suppressor cells in rats. 623 67

Splenic lymphocytes from cytomegalovirus-infected mice lost their in vitro proliferative responses to cytomegalovirus antigen within 3 h after in vivo treatment with antilymphocyte globulin and prednisolone. The response was inhibited when the agents were administered separately or together, and inhibition persisted through a 2-week course of immunosuppression. Circulating specific antibodies were depressed by multiple injections of antilymphocyte globulin alone or with prednisolone, but not by prednisolone alone. Mitogen-induced blast transformation was immediately depressed by immunosuppression with both agents. Although the response to lipopolysaccharide returned briefly, it declined with continuing treatment. Cytomegalovirus infection augmented the depressive effect of immunosuppression on the lipopolysaccharide proliferative response. Prednisolone treatment of infected animals did not affect the concanavalin A response, and lipopolysaccharide stimulation decreased more slowly and to a lesser extent than it did in mice treated with antilymphocyte globulin or both agents. Loss of specific cell-mediated immunity and simultaneous depression of humoral immunity indicated that immunosuppression immediately created an inability to respond to an active cytomegalovirus infection.
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PMID:Immediate loss of cell-mediated immunity to murine cytomegalovirus upon treatment with immunosuppressive agents. 626 40

Inbred RIII mice, known to be infected neonatally with murine mammary tumor virus so that females develop mammary adenocarcinoma by 12-15 months of age, were examined with regard to antisheep red blood cell antibody responses at the cellular level. Female mice, 3-11 months old, compared to male mice of the same ages had consistent and significant depression of the antibody response of their splenocytes. Furthermore, female mice with adenocarcinoma showed an even greater depression of the antibody response. Spleen sizes were consistently increased in females as compared to those of male mice throughout the first year of life. The blastogenic responsiveness of the splenocytes to the B-cell mitogen Escherichia coli lipopolysaccharide and the T-cell mitogen phytohemagglutinin-P was not significantly different between male and female mice during the same periods, although the responses of the older tumor-bearing female mice to phytohemagglutinin-P were lower than those of non-tumor-bearing female mice. A complex relationship between age, sex, and immune responsiveness was evident in these mammary tumor virus-infected mice, which made it difficult to attribute a specific immune event to emergence of the mammary adenocarcinomas in the female as compared to male mice.
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PMID:Age- and sex-related differences in antibody formation and blastogenic responsiveness of splenocytes from RIII mice developing virus-induced mammary adenocarcinoma. 627 37


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