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)

In the present study we observed a significant depression of thymocytes during pregnancy and investigated the influences of this thymic change on the immunologic capacities of peripheral lymphocytes. Thymocytes in pregnant mice began to decrease in number from Day 10 and reached about 0.1-fold of the nonpregnant level at Day 19, just before parturition. At late stage of pregnancy, thymocyte subpopulation expressing CD4+CD8+ and Thy1.2+PNA+ was selectively depressed. On the contrary, peripheral lymphocytes including splenocytes, peripheral blood lymphocytes and peripheral lymph node cells showed no depression. As to the immunologic capacities of the pregnant hosts, delayed footpad reaction and phagocytic activity of fixed liver macrophages in vivo were remarkably suppressed, but MLR reactivity and antibody response to SRBC or haptens were well preserved. Transfer of pregnant sera or administration with steroid hormones especially E3 into nonpregnant mice induced similar changes in the thymus and peripheral lymphocytes in number and subsets but this could not mimic the immunologic reactivities of the pregnant mice. These results suggest that sex steroid hormones such as E3 play an important role in the changes in cell populations of each lymphoid organ and the immune reactivities of the hosts during pregnancy. However, other factors also contribute to the immunologic capacities of the maternal hosts.
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PMID:Thymic depletion in pregnancy: kinetics of thymocytes and immunologic capacities of the hosts. 166 37

Prothymosin alpha [corrected] (ProT alpha) and thymosin beta 4 [corrected] (T beta 4) were isolated from murine thymus and characterized by microsequence analysis. Murine T beta 4 has an identical sequence to bovine T beta 4, whereas murine ProT alpha is highly homologous to rat Pro T alpha. Murine Pro T alpha differs from rat Pro T alpha at two positions, Glu100 and Asp108 of the rat sequence are substituted by aspartic and glutamic acid, respectively, in murine Pro T alpha. The amount of Pro T alpha in murine thymus was found to be reduced after in vivo treatment with staphylococcal enterotoxin B [corrected] (SEB), a superantigen which stimulates T cells bearing specific V beta receptors. Results from the anti-SRBC (sheep erythrocyte) plaque-forming cell assay showed that the antibody response of the spleen cells from these animals was also suppressed. On the other hand, the amount of T beta 4 was not changed significantly. Our studies suggest that the suppression of SEB on antibody response correlates with the depression of Pro T alpha production in the thymus.
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PMID:Depression of prothymosin alpha production in murine thymus correlates with staphylococcal enterotoxin-B-induced immunosuppression [corrected]. 222 39

Six week old Swiss mice were sensitized by subcutaneous injection of 10(7) sheep red blood cells without adjuvant. One hour after sensitization, the mice were treated with erythromycin lactobionate for ten days. The minimal (15 mg/kg/day) and maximal (57 mg/kg/day) doses clinically used were assayed. The daily dose of erythromycin was administered intraperitoneally, in two injections, one every 12 hours. The kinetics of delayed type hypersensitivity reaction, measured by means of the foot-pad test, was evaluated by challenging different groups of fourteen mice with an eliciting dose of 10(8) SRBC injected into the foot-pad on days 1, 2, 3, 4, 5, 6, 7, 8, 9 and 10 after sensitization. Total and 2-mercaptoethanol resistant haemagglutinating antibody titres were determined in sera obtained from mice immediately after measuring the delayed type hypersensitivity reaction. Treatment with maximal erythromycin dose gave rise to a significant enhancement of the cellular immune response, and also to an acceleration of the humoral antibody response. On the other hand, treatment with minimal erythromycin dose gave rise to a slight depression of the immune cellular response and also to a depression of the antibody production at the beginning of the humoral response.
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PMID:Effect of erythromycin treatment on specific immunologic response in mice. 263 37

Spleen cells from CBA/J mice infected with Neisseria meningitidis displayed depressed in vitro plaque-forming cell (PFC) responses to T-dependent (sheep red blood cell; SRBC) and T-independent (TNP-LPS, TNP-Ficoll) antigens. The inhibition was observed over a wide range of antigen concentrations. The decreased responsiveness of splenocytes from infected mice was due to a selective impairment of B-cell function since helper-T-cell activity was intact in infected mice as shown by the ability of T-enriched lymphocytes to cooperate with normal B-enriched lymphocytes in the generation of an anti-SRBC response, accessory macrophage function was preserved since adherent spleen cells from bacteria-injected mice were shown to produce normal or increased levels of IL-1 and were able to cooperate with normal non-adherent spleen cells in the generation of PFC against SRBC. Addition of peritoneal cells from normal animals or extraneous IL-1 both failed to restore normal PFC responses in cultures of splenocytes from infected mice. Finally, B-enriched lymphocytes from infected mice produced poor anti-SRBC responses when cultured with either Con A supernatant or T-enriched lymphocytes from normal or infected mice. Cell-mixing experiments failed to detect the presence of suppressor cells in cultures of unfractionated spleen cells or B-enriched lymphocytes from infected mice. Therefore, the immunological unresponsiveness associated with a Neisseria meningitidis infection was attributed to a meningococcus-induced defect(s) in B-cell function. In vivo polyclonal B-cell activation leading to clonal exhaustion did not play a major role in the depression of humoral responses since meningococcal infection induced little or no polyclonal Ig secretion.
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PMID:Selective impairment of B cell function by Neisseria meningitidis. 294 9

Experiments were undertaken to determine whether the depression of natural killer (NK) activity previously observed in the peripheral blood lymphocytes (PBL) of leukaemia patients in remission extended to NK-like precursors in the blood. T-lymphocytes (E+) from leukaemia patients and normal subjects were depleted of IgG Fc-receptor-bearing (gamma FcR) fresh NK cells by passage over immune complex-coated monolayers. gamma FcR - E + PBL were cultured alone or with DAUDI cells. On day 5 of culture, cytotoxicity toward the NK-sensitive cell lines K562 and MOLT-4 was evaluated in the responder lymphocytes of leukaemia patients and controls. Negligible NK-like cytotoxicity was found in both FcR - E + PBL responder populations cultured alone. By contrast, stimulation with DAUDI induced high levels of K562 and MOLT-4 cytotoxicity in leukaemia as well as in normal responder cells. Complement-mediated cytotoxicity experiments using various McAb demonstrated that in both normal and leukaemia cultures NK-like effectors react with the pan-T OKT3 McAb and with the OKT11 McAB directed to the SRBC receptor, but not with Leu 1 1b and OKM1 McAbs, directed against antigens expressed on peripheral blood NK cells. Fractionation of the responder cells on discontinuous Percoll gradients showed that most of this activity was present in the highly dividing blast cell fraction.
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PMID:Generation of non MHC restricted killing in non-cytotoxic T-lymphocytes from leukaemia patients. 295 Sep 19

A tissue-culture system to stimulate human peripheral blood mononuclear cells (PBMC) has been employed in which IgM plaque-forming cell (IgM PFC) generation in response to sheep erythrocytes (SRBC) is dependent on macrophages and T suppressor and helper lymphocytes. In this system PBMC from normal subjects give IgM PFC responses ranging from 26 to 938 PFC/culture. Heat-aggregated human IgG or immune complexes present for the duration of culture induce a significant depression of PFC. Unaggregated IgG has no effect on the response or only a moderate stimulatory effect at the highest dose. The results of these experiments are compatible with previous results in a murine system, which indicated that Fc gamma receptor-positive (Fc gamma R+) cells in the suppressor subset are the target for aggregated IgG and induce depression of the PFC response. A similar mechanism may be operating in the human system described here, although the target cell has not been identified. These results may reflect a mechanism of immunomodulation dependent on interaction of Fc receptor (FcR) ligands with FcR, which may play a role in the pathogenesis of immune complex disorders.
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PMID:Depression by Fc gamma receptor ligands of SRBC-induced IgM-PFC generation in human blood mononuclear cell cultures. 297 32

The influence of an infection with P. chabaudi adami on the isotypic distribution of the in vivo antibody response to SRBC was investigated. Previous experiments suggested that the IgG1 isotype was poorly represented in the antibody response to plasmodial antigens and in the non-specific B cell response which accompanies an infection with P. chabaudi. The experiments described here indicated that although the magnitude of the total primary or secondary in vivo PFC response to SRBC was relatively unaffected by infection, the SRBC-specific IgG1 PFC response was depressed. Maximum depression of the IgG1 component of the response was observed when the priming dose of SRBC was administered at the same time as or after infection with P. chabaudi organisms. Coincident with the depression in the IgG1 response in infected mice was a corresponding increase in the SRBC-specific IgM response. The IgG1 depression was not a consequence of different kinetics of the generation of an IgG1 response, since at all times measured, the IgG1-PFC response was lower. In addition, the depressed IgG1 responses occurred only during a viable infection and could not be induced by inoculation of large amounts of irradiated erythrocytic stages of the parasite. These data suggest therefore, that there is a selective depression of IgG1 antibodies (but not those of other isotypes) regardless of antigenic specificity as a result of infection of C57BL/6 mice with P. chabaudi adami.
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PMID:Influence of Plasmodium chabaudi adami on the isotypic distribution of the antibody response of mice to sheep erythrocytes. 331 75

The immune responses to SRBC and LPS were examined in immunized and non-immunized inbred cotton rats at different times after an infection with Litomosoides carinii. During the infection, the T-cell dependent immune response to SRBC was significantly suppressed in non-immunized animals as compared to non infected controls. In contrast, after immunization with SRBC the antibody levels of infected animals were significantly higher in three of five events. At the onset of patency the response to SRBC was significantly depressed transiently in immunized animals. A corresponding depression could be provoked by injections of isolated microfilariae as well as by FCS in immunized animals, infected and non-infected. The level of the antibodies was dependent on the density of microfilariae in the peripheral blood. The T-cell independent response to LPS was equal in non-immunized infected animals as in controls. After immunization with LPS during prepatency and at onset of patency a distinct but commensurate reaction was observed. Only after immunization at the peak of patency, the immune response of infected animals was significantly suppressed. In general, the antibody levels to LPS were not influenced by the microfilaremia.
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PMID:T-cell dependent and T-cell independent immune response in normal and in with Litomosoides carinii infected cotton rats. 355 Oct 26

The humoral immune response to SRBC and contact sensitivity (CS) reaction to picryl chloride and oxazolone was studied in traumatized mice (laparotomy, gastrectomy, leg amputation). While depression of CS was observed after leg amputation and gastrectomy, laparotomy had no effect. On the other hand, laparotomy and gastrectomy evoked stimulation of anti-SRBC antibody production, whereas leg amputation significantly reduced the humoral response. Results are discussed in relation to postulated role of trauma in the modulation of immune response regarding the anatomic localization and extent of surgical procedure.
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PMID:Influence of anatomic localization and extent of surgical trauma on immune responses in mice. 406 13

High-pressure oxygen (HPO) therapy for Pseudomonas aeruginosa infections of burn wounds has not been as effective as in vitro studies predicted. Mitigation of HPO toxicity for P. aeruginosa by nutrients present at the burn site could explain the lack of in vivo success. Alternatively, HPO-induced depression of host defense mechanisms could negate beneficial effects arising from HPOs known toxicity for P. aeruginosa. Accordingly, mouse peritoneal exudate cells (PEC), preincubated for 24 h in 1 atm of air-CO(2), were used to study the in vitro effects of HPO or air-CO(2) on phagocytosis of P. aeruginosa or sheep erythrocytes (SRBC). Subsequent 2-h exposures of PEC to increasing numbers of bacteria, in an air-CO(2) atmosphere, decreased the percentage of bacteria cleared as well as PEC viability. Similar exposures of PEC to bacteria in an HPO atmosphere prevented the loss of PEC viability and increased bacterial clearance. In control experiments, increasing the number of SRBC relative to PEC decreased the percentage of SRBC cleared without decreasing PEC viability, as determined under air-CO(2); short (2 h) exposure to HPO did not affect SRBC clearance. Microscopic examination of PEC indicated that a 24-h preincubation in HPO decreased the percentage of PEC which could ingest SRBC during subsequent experimental exposures (2 h) to air-CO(2) or HPO. These data suggest that short periods of exposure to HPO promote the ability of PEC to clear pseudomonads by adversely affecting the bacteria. This in turn prevents a pseudomonad-induced depression of PEC viability and function. In contrast, prolonged HPO exposure may be detrimental to phagocytic activity.
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PMID:Inhibition of Pseudomonas aeruginosa by hyperbaric oxygen: interaction with mouse peritoneal exudate cells. 421 74


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