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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The traffic of lymphocytes through lymphoid tissues is of importance in both the initiation and development of the immune response. The effects of lidocaine on lymphocyte traffic through primary peripheral lymph nodes of sheep (popliteal and pre-femoral) was investigated by three routes of lidocaine administration. Infiltration of lidocaine above the study node and as the sole anesthetic agent for study node efferent lymphatic cannulation produced mild depressions in lymphocyte outputs into study node efferent lymph. This depression was comparable to that encountered with regional epidural anesthesia for similar operations, but was significantly less than that associated with general anesthesia (P less than 0.000015). In animals with established chronic cannulation of study node efferent lymphatics, both study node drainage area injection of lidocaine and systemic administration of lidocaine (intravenously by bolus injection at a distant site) produced prompt and sharp depressions in lymphocyte traffic as mirrored in the output of lymphocytes into study node efferent lymph. The output of both small recirculating lymphocytes and of blast lymphocytes was affected.
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PMID:Lymphocyte traffic effects of systemic and local lidocaine in sheep. 376 34

The correlation between the level of stress-induced natural killer (NK) depression and glucocorticoid binding to specific spleen cell receptors and hormonal profile in inbred mouse strains (CBA, BALB/c, C57BL/c, A/Sn) has been investigated. Stable interstrain differences in stress-induced natural killer activity and glucocorticoid receptor binding (Bm and Kd) have been revealed. It was demonstrated that the mechanism of NK activity depression during stress consists in genetically determined potential sensitivity of lymphoid cells to physiological fluctuations of glucocorticoid levels. This made it possible to identify stress-resistant and stress-sensitive mouse strains.
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PMID:[Interstrain differences in cellular glucocorticoid reception in mice and the degree of suppression of normal killer activity during immobilization stress]. 382 99

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

When BALB/c mice (young and adult animals of both sexes) were infected intraperitoneally with 10(3) viable cells of Francisella tularensis (10(2) 50% lethal dose), all mice in these groups died on day 4. Reductions in thymus weights and in numbers of thymic cortex lymphocytes were observed in all the groups, but the decline was not so severe in the young females. Increases of plasma corticosterone in the adult males began 1 day after infection, but in the young females, the levels did not increase until day 3, the same days on which the respective thymus weights began to decline. Depletion of the thymus weights in the infected mice was prevented by adrenalectomy. The lymphocytes of the thymus (T)-dependent areas in peripheral lymphoid tissues in all groups were destroyed. By using an electron microscope, we found a large quantity of F. tularensis within the macrophages in the T-dependent areas but not in the thymus. The destruction of lymphocytes in the T-dependent areas was not prevented by adrenalectomy. Therefore, it was concluded that the weight reduction of the thymus is due to the stress of the F. tularensis infection. However, we think other mechanisms are responsible for the depression of lymphocytes in the T-dependent areas of peripheral lymphoid tissues.
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PMID:Weight reduction of thymus and depletion of lymphocytes of T-dependent areas in peripheral lymphoid tissues of mice infected with Francisella tularensis. 387 62

Groups of C57BL/6J, male mice were exposed to 300 ppm benzene via inhalation for 115 exposures (6 h/day, 5 days/week), a regimen known to cause thymic lymphoma in these animals. The effects of these exposures on lymphoid parameters were determined by measuring the numbers of B- and T-lymphocytes and mitogen-induced proliferation of B- and T-lymphocytes in bone marrow, spleen, and thymus after 6, 30, and 115 exposures. The numbers of B-lymphocytes in bone marrow and spleen and the numbers of T-lymphocytes in thymus and spleen were found to be markedly reduced after all 3 periods. Mitogen-induced proliferation of bone marrow and splenic B-lymphocytes exhibited a progressive depression throughout the exposure period reaching a point of no observable response after 115 exposures. Splenic T-cell mitogen-induced proliferation was also markedly depressed throughout the exposures, but there was no evidence of a progressive decline in this response during the exposures. Bone marrow cellularity increased 3-fold and the numbers of thymic T-cells increased 15-fold in benzene-exposed mice between the 6th and 30th exposure. No corresponding increase in splenic cells was observed in benzene-exposed mice during this interval. The marked increases in the numbers of cells in bone marrow and thymus are interpreted as arising from compensatory proliferation of a subpopulation of cells in response to the exposures. The absence of increases in cell number in the spleen is interpreted as reflecting the lack of lymphoid restorative capacity in this organ. The marked increases of thymic and bone marrow cellularity are discussed relative to the known ability of this benzene exposure regimen to produce thymic lymphoma in these animals.
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PMID:Protracted exposure of C57BL/6 mice to 300 ppm benzene depresses B- and T-lymphocyte numbers and mitogen responses. Evidence for thymic and bone marrow proliferation in response to the exposures. 387 53

Acute mixed myeloid-lymphoid leukemia is uncommon. We report four cases in which myeloid and lymphoid cell markers were observed simultaneously or sequentially when 94 patients with acute leukemia were phenotyped according to the French-American-British (FAB) classification system, with cytochemical stains, and with immunologically defined differentiation markers (identified by monoclonal antibodies and antiterminal deoxynucleotidyl transferase [TdT]). In one case, conversion from acute lymphoblastic leukemia to acute myeloid leukemia was noted (FAB L1, TdT+ to FAB M4, Auer rods, TdT-). In another patient, two distinct populations of myeloid and lymphoid blast cells were observed simultaneously (TdT-, LeuM1+/TdT+, LeuM1-). In two additional patients, acute leukemia was characterized by the expression of both lymphoid and myeloid markers on the same cell (TdT+/Leu M1+, B4+/Leu M1+ and greater than or equal to 70% TdT+, T11+, My9+). The Philadelphia (Ph1) chromosome was negative in all cases, though other chromosomal abnormalities were noted in three out of four cases. Malignant transformation of a pluripotential stem cell for both lymphoid and myeloid lineages, with or without the Ph1 chromosome marker, could explain the coexistence of distinct populations of lymphoblasts and myeloblasts in acute leukemia. Acute leukemia with a biphenotypic profile may reflect genome depression accompanying neoplasia.
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PMID:Simultaneous or sequential expression of lymphoid and myeloid phenotypes in acute leukemia. 388 Jun 43

The interdependence between immunologic events occurring within acutely rejecting rat cardiac allografts and those in host lymphoid tissues were studied. To evaluate cellular dynamics of allograft infiltration, 111In-labeled thoracic duct lymphocytes from Lewis rats were administered intravenously daily (0 to 7 days after transplantation) to (Lewis X BN)F1 heart-grafted unmodified Lewis rats, sacrificed 24 hours later. Accumulation of thoracic duct lymphocytes in the allografts peaked 4 to 5 days after transplantation. To evaluate whether these changes at the graft site were sufficient to carry on the rejection response in the absence of a sustained host immunologic drive, acutely rejecting (Lewis X BN)F1 cardiac allografts were retransplanted serially at days 1 through 5 into normal syngeneic animals. All these regrafts survived greater than 100 days. Neither infusion of interleukin-2-conditioned medium (100 IU for 7 days intravenously) into regrafted hosts nor preoperative perfusion of the retransplanted hearts with interleukin-2-conditioned medium (300 IU) could complete the rejection process. Using flow cytometry analysis, we then assessed the phenotypic alterations of the mononuclear cells infiltrating the graft. The ratio of T helper: T cytotoxic/suppressor cells, which at day 3 was 1.57, inverted abruptly to 0.67 by days 5 to 6. After retransplantation a dramatic depression in T-lymphocyte subsets occurred, particularly affecting the T cytotoxic/suppressor phenotype. Trafficking studies revealed that the T cells that left the regrafts migrated mainly to spleen and mesenteric lymph nodes and away from bone marrow and peripheral blood of the syngeneic secondary recipients. Finally, histologic manifestations of acute rejection at days 4 to 5 virtually reversed themselves after regrafting. These studies emphasize the systemic nature of the rejection cascade, which depends fully on the host lymphoid system; even late changes in the graft microenvironment are not sufficient to produce final immunologic destruction.
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PMID:Host-graft relationship: the systemic nature of allograft rejection. 389 38

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
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PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

Tumor-infiltrating lymphocytes (TIL) from human pulmonary tumors have been studied as a model for local depression of cell-mediated immunity at the tumor site. To better characterize these lymphoid infiltrates, a new method of lymphocyte extraction of high yield and purity was developed. The TIL from 11 human lung tumors of varying histologic types were prepared. After mechanical disaggregation to a single cell suspension, the TIL, contaminated with tumor cells and macrophages, were incubated with carbonyl iron to deplete macrophages. Further purification was performed in a unit gravity sedimentation apparatus utilizing a continuous 2-4% Ficoll gradient. Usable TIL recovery was 41.2 +/- 7.7% of input cells and was minimally contaminated by tumor cells and macrophage/monocytes. The high yield and purity of TIL preparations have resulted in a higher proportion of tumors suitable for immunological analysis. An example of the type of experiments possible with such preparations is shown.
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PMID:A method for improved yield and purity in extracting lymphocytes from lung tumors. 396 5

The influence of cyclophosphamide (CY) pretreatment upon the development of tuberculin hypersensitivity has been studied during the course of infection of mice with BCG. An enhancement of the DTH response to BCG antigens occurred during the induction phase, whereas a depression of this response occurred at the peak and during the decay phase of sensitization. The development of the early DTH-promoting and of the late DTH-depressing effect of CY was favoured by the use of a supra-optimal dose of BCG. Both these effects were cell-dependent since they could be transferred adoptively to syngeneic recipient mice with sensitized lymphoid cells but not with specific immune sera. Pretreatment with CY favoured the emergence of cells capable of responding in vitro to BCG antigens in the draining lymph nodes of BCG-infected mice. No simple association however, exists between this in vitro lymphocyte transformation response and the DTH response.
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PMID:Opposite effects of cyclophosphamide pretreatment on tuberculin hypersensitivity during the course of sensitization of mice with Mycobacterium bovis BCG. 404 94


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