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)

Mitogen stimulation of cells from various lymphoid organs of C3H/He mice chronically infected with an isolate of Trypanosoma congolense was studied at different time intervals after infection, using concanavalin A (Con A) and lipopolysaccharide (LPS). At the same time, changes in the percentages of T, B and null lymphocytes in these organs were determined by immunofluorescence staining. The responses of T and B lymphocytes in the spleen were totally depressed, and the cellular composition was drastically altered by day 14 after infection. Unlike the spleen, the lymph nodes showed minor changes in their T and B lymphocyte responses and cell composition during the course of the infection, except the B cell response and composition which were altered late in the infection. The thymus and bone marrow did not show any appreciable changes in their mitogen responses and cell composition throughout the infection. The peripheral blood lymphocytes showed reduced B cell responses. Spleen cells from chronically infected mice suppressed lymphocyte stimulation induced in normal spleen and lymph node cell populations by Con A, LPS and allogeneic stimulator cells. Lymph node cells from the same group of mice did not exhibit any such suppressor activity. In the experimental system used here, the spleen is the primary site of immune depression, and other lymphoid organs such as the lymph nodes and thymus are very little affected.
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PMID:Immunodepression in trypanosome-infected mice. VI. Comparison of immune responses of different lymphoid organs. 645 82

Spleen and mesenteric lymph node cell blastogenic responses to the mitogens concanavalin A and lipopolysaccharide and to parasite antigens were examined in vitro following removal from mice undergoing primary or secondary infection with Nippostrongylus brasiliensis. During primary infection spleen cells showed a marked increase in proliferative responsiveness to both mitogens, followed by a marked depression thereafter. During a secondary infection the response of spleen cells to both mitogens remained depressed. In contrast, cells from the mesenteric lymph nodes of infected mice exhibited enhanced responsiveness to Con A and LPS, followed by depression of the response, followed by another cycle of enhancement upon reinfection. Sensitivity of both spleen and especially mesenteric lymph node cells to Nb antigens was greatest at approximately the time of worm expulsion: Day 13 after primary and Day 8 after secondary infection.
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PMID:Modulation of lymphoid cell blastogenic responsiveness to mitogens by Nippostrongylus brasiliensis infection. 703 66

In BALB/c mice, the injection of pristane resulted in a severe decrease in splenic T and B cell proliferative responses to mitogens and in a depression of natural killer (NK) activity. The effects of T and B cells, which persisted for at least 5 mo, were mediated by different mechanisms. T cell responsiveness to PHA dropped significantly below control levels 1 wk after the first of three monthly pristane injections, whereas B cell proliferation in response to LPS did not decrease until 4 wk after the first injection. The removal of plastic-adherent suppressor cells completely restored T cell proliferative capacity, but had no effect on B cells. NK activity against YAC-1 tumor targets was reduced 1 mo after the first pristane injection and remained depressed for at least 3 mo. This depression was not mediated by plastic-adherent suppressor cells. Spleen cell NK activity from pristane-treated mice could not be augmented by the interferon inducer Poly I:C to the same extent as that of control mice. This suggests an effect of pristane on either pre-NK cells or on cells that regulate NK activity.
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PMID:Depression of natural killer activity and mitogen responsiveness in mice treated with pristane. 714 8

Serum adenosine deaminase (ADA) of 74 liver cirrhosis patients and 100 healthy subjects as control were examined with improved Martinek microassay and peripheral T lymphocyte subsets of 38 liver cirrhosis patients and 60 healthy subjects studied by indirect immunofluorescence assay (IFA) for exploring the relationship between them and syndrome types of TCM. The result showed that level of ADA of liver cirrhosis patients was higher than that of control (P < 0.01) and increased in following order: the type of Liver-energy Depression and Spleen Deficiency, that of Heat-Stagnation and Blood Stasis and that of Yin-Deficiency and Microvessel Obstruction. The difference of serum ADA among the types were significant (P < 0.01). The result also showed that OKT8 of liver cirrhosis patients was higher, the ratio of OKT4/OKT8 was lower than the healthy subjects (P < 0.05-0.01), but the difference among the types were not significant (P > 0.05). Serum ADA seemed to be one of the reference indexes in differentiating syndrome types of TCM, determining the patient's condition and prognosis.
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PMID:[Correlation between serum adenosine deaminase, peripheral T lymphocyte subsets and syndrome types of traditional Chinese medicine in liver-cirrhosis patients]. 795 Jan 82

The oral administration of CII by gavage to WA/KIR rats before a conventional arthritogenic challenge with bovine CII in FIA reduced the incidence (by 23%) and delayed the onset of collagen-induced arthritis in about 50% of the animals. Selective changes in B cell and T cell responses to CII in animals treated this way are interpreted to indicate a state of tolerance or hyporesponsiveness to CII. Tolerant animals made less serum antibody, to bovine and rat CII, of the IgG2b isotype and more of the IgG1 isotype. Phenotypic and functional analysis of peripheral lymph node cells showed that those from tolerized animals expressed less MHC Class II, proliferated less and secreted less IgG2b anti-CII antibody in response to stimulation in vitro with CII when compared with cells from non-tolerant animals. However, this depression of the immune responses to CII seen in vitro was overcome when the cells were incubated with increasing amounts of CII. Tolerance could be transferred to normal animals. Spleen cells, and nylon wool-filtered splenic T cells (but not mesenteric lymph node cells) adoptively transferred hyporesponsiveness to normal recipients which were then less susceptible to collagen-induced arthritis. Transfer of serum from gavaged animals did not modify the susceptibility of normal recipients to arthritis. Spleen cells from gavaged animals suppressed proliferative and antibody responses in co-cultures in vitro with lymph node cells from animals immunized with CII in FIA. The suppressive spleen cell population contained more cells expressing MHC Class II, in both the CD8+ and CD4+ populations. These studies show that the oral administration of CII alters the subsequent immune response to the arthritogenic challenge and indicate that this oral tolerance of CII is due, not to clonal deletion or anergy, but rather to an antigen-driven active suppression mechanism that affects both T cells and B cells, most likely through the action of regulatory cytokines IL-4, IL-10 and TGF beta.
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PMID:Suppression of collagen induced arthritis by oral administration of type II collagen: changes in immune and arthritic responses mediated by active peripheral suppression. 800 14

Depression of the cellular immune response to Toxoplasma gondii has been reported in both mice and humans. The present study was undertaken to determine the kinetics and mechanism of the observed downregulation of interleukin 2 (IL-2) production during experimental murine toxoplasmosis. For these investigations, the cell-mediated immune response to the wild type (PTg) was compared with that to the less-virulent mutant parasite (PTgB), which is deficient in the major surface antigen, p30 (SAG-1). Spleen cells from infected A/J mice failed to proliferate in response to Toxoplasma antigens during the first week of infection. Both PTg- and PTgB-infected A/J mice exhibited a significant reduction in the concanavalin A (Con A)-induced lymphoproliferative response. Further, the response of splenocytes from mice infected with the wild-type parasite was significantly diminished compared with that of mice infected with PTgB. The lymphoproliferative response to Con A reached its nadir at day 7 and remained below control levels for at least 14 days postinfection. By day 21 postinfection, the response to Con A and to Toxoplasma antigens was restored to the level observed prior to day 7. Con A-stimulated culture supernatants of spleen cells from mice on day 7 postinfection contained significantly less IL-2 than normal mice. There was no significant difference in the numbers of binding sites or capacity of high-affinity IL-2 receptors between infected and normal mouse splenocytes as determined by Scatchard analysis. Exogenous IL-2 at different concentrations failed to restore the proliferative response of lymphocytes from infected mice to Con A. Adherent macrophages from 7-day-infected mice were able to suppress IL-2 production by normal splenocytes following stimulation with Con A. The inhibitory activity mediated by infected cells was reversed by the antibody to IL-10 but not transforming growth factor beta. There were insignificant levels of nitric oxide production in both infected and normal splenocytes. These results indicate that during acute murine toxoplasmosis, there is a well-defined period (day 7) during which both the T-cell mitogen and parasite antigen-associated lymphoproliferative response are reduced. Further, there is a reduction in the production of IL-2 and an increase in IL-10, which appear to mediate, in part, the observed downregulation of immunity to T. gondii.
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PMID:Impairment of the cellular immune response in acute murine toxoplasmosis: regulation of interleukin 2 production and macrophage-mediated inhibitory effects. 800 79

Natural killer (NK) cells are thought to play an important role in the control of metastatic dissemination. Therefore, stimulation of cytotoxic activity of NK cells against neoplastic cells could be preventive for metastatic spread. Bomirski amelanotic (Ab) melanoma of Syrian hamster is a transplantable tumor metastasizing preferably to the kidneys. During growth of the melanoma a significant depression of cytotoxic activity of NK cells of tumor hosts is observed. Treatment of melanoma-bearing hamsters with indomethacin provided in drinking water resulted in the increase of NK cytotoxic activity of blood cells and in the lower occurrence of kidney metastasis. Spleen cells obtained from healthy and melanoma-bearing hamsters were cultured in vitro with agents influencing NK activity. We found an augmentative effect of human interleukin 2 (IL2) and human tumor necrosis factor (TNF). We also observed the synergistic effect of IL2/TNF combination, which was present in both groups of animals. The stimulatory effects of cytokines could be potentiated by the additional supplementation of cultures with indomethacin. Similar experiments were performed on spleen cells isolated from the healthy and tumor-bearing animals treated in vivo with indomethacin. Also, in this group of hamsters in vitro stimulation of NK cell activity by the cytokines was effective. The studies presented may give insight into the pathogenesis of immune abnormalities seen in advanced stages of progression of Ab melanoma, and can provide an experimental basis for immunomodulation in this tumor model of spontaneous metastasis.
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PMID:Indomethacin inhibits kidney metastasis in bomirski melanoma-bearing hamsters, and modulates natural killer cytotoxic activity of tumor hosts in vivo and in vitro. 985 38

Spleen veins ligature (SVL) led to acute congestive splenomegaly in rats with subsequent normochromic anaemia disappearing on the 21st day after the SVL. An appreciable depression of the bone marrow erythropoiesis, particularly of the so called "proliferating erythroblastic islets" number, was evident on the 7th and 14th days of post-SVL period. The post-SVL anaemia was also associated with occurrence of the "islets" missing central macrophages and eosinophil-enriched "islets" in bone marrow.
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PMID:[Effect of acute congestive splenomegaly on erythropoiesis in rats]. 1138 59

Tumor development and aging can each alter immune competence. The present study aimed to determine the impact of Lewis lung carcinoma (LLC) presence on immune parameters of middle-aged (averaging 6.5 months) versus aged (averaging 21.3 months) mice. An age-associated decline in the CD4+ cell frequency was seen in freshly isolated spleen and lymph node cells, as well as in cultures stimulated with immobilized anti-CD3. This decline was not further exacerbated by tumor presence. What was prominently inhibited by tumor was the capacity of either splenic or lymph node CD4+ cells to become stimulated to express IFN-gamma. Spleen and lymph node cultures from aged tumor-bearing mice had the lowest frequency of CD4+IFN-gamma+ cells and the least amount of secreted IFN-gamma. CD8+ cells were not affected by aging, but tumor presence reduced the induction of CD8+IFN-gamma+ cells in lymph node cultures. We previously showed that LLC growth stimulates myelopoiesis, as seen by splenomegaly and the mobilization of immune inhibitory CD34+ progenitor cells. Tumor presence in middle-aged mice reduced spleen cell blastogenesis, which was mediated by CD34+ cells. Aged mice had reduced blastogenesis, and this was further reduced by presence of tumor. However, neither the age-associated immune dysfunction nor the tumor-induced immune suppression in aged mice was due to CD34+ progenitor cells. These studies show how tumor presence can further compromise the immune dysfunction that accompanies aging. In addition, they show that aging impacts on the mechanisms by which tumors inhibit T-cell capabilities, with myelopoiesis-associated CD34+ cells mediating the immune depression of middle-aged tumor-bearers and an independent mechanism being responsible for the immune depression in aged tumor-bearing mice.
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PMID:Impact of aging on immune modulation by tumor. 1157 May 85

The visceral and the different spectrum of cutaneous leishmaniases have been incriminated to be among the opportunistic infections co-existing with HIV/AIDS. In co-infections, leishmaniases surface in high prevalence, present frequently atypically, pose difficulties to be detected by routine diagnostic tests, most often result in an unfavorable response to treatment, frequent relapses and in premature deaths. Such presentations and management difficulties shall be highlighted in this review. To extract information on the scope of manifestations and responses to management, literature was surveyed utilizing the Pub Med electronic literature search. In due course, pertinent characteristics surfacing in HIV/AIDS and leishmaniasis co-infections comprising of clinical presentations and parasitological and serological findings were tracked. Investigation options, management approaches, outcomes of various treatment regimen and other intervention strategies were as well explored. Visceral leishmaniasis and HIV-1 are both associated with a depression of T cell response and similar disturbances of cytokine networks. The appearance of HIV has led to numerous atypical clinical manifestations of leishmaniasis among immunocompromised patients to include, recurrences, lingual, cervical, esophageal, mucocutaneous and presentations in other unusual sites. The common clinical presentations of the disease might not always be present being masked by other associated opportunistic infections. Spleen aspiration is more sensitive in immuno-competent visceral visceral leishmaniasis suspects, however, bone marrow aspirate remains the safest and the most frequently employed diagnostic technique in co-infected patients. Several species of Leishmania are incriminated in affecting HIV infected subjects, including formerly unknown zymodemes. In spite of the high number of reported cases of HIV-related VL, the treatment of choice, the best dosage and the duration of therapy appear not to be properly established. The pentavalent antimonials still remain the first line of therapy for co-infected cases. Amphotericin-B, especially the liposome formulation (Ambisome) was found to be relatively less toxic and more potent compared to pentamidine. A broad spectrum of other drugs have as well been used. The widespread use of HAART are envisaged to contribute to a progressive decrease in the morbidity and mortality of HIV-associated visceral leishmaniasis. There is no effective chemoprophylaxis or immuno-prophylaxis to prevent leishmanial infection. In the events of co-infections with HIV/AIDS, the need for policy provisions to control both diseases needs to be underlined. It is as well of a paramount importance that factors influencing co-infection are understood for effective treatment against leishmaniasis in co-infected patients. The need for improved diagnostic tests and new more effective and less toxic drugs is also apparent.
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PMID:Leishmaniases and HIV/AIDS co-infections: review of common features and management experiences. 1280 30


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