Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024312 (lymphopenia)
 4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The natural resistance of adult specific-pathogen-free cats to feline leukemia virus (FeLV) was abrogated by treatment with various doses of a synthetic corticosteroid, methylprednisolone acetate (MPA), prior to either oral-nasal or i.p. inoculation of FeLV. Persistent viremia was induced in 82% (18 of 22) of MPA-treated cats versus 11% (1 of 9) of age-matched control cats. MPA-treated FeLV-inoculated cats developed prolonged lymphopenia (2 to 8 weeks postinoculation) and a delayed antibody response to the feline oncornavirus-associated cell membrane antigen. The distribution of FeLV group specific antigen in tissues of MPA-treated, FeLV-inoculated cats suggested that corticosteroids enhanced susceptibility to FeLV by impairing early viral containment in the reticuloendothelial and lymphoid tissues.
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PMID:Influence of adrenal corticosteroids on the susceptibility of cats to feline leukemia virus infection. 22 25

Mice injected with a single well tolerated dose of hydrocortisone acetate were observed over 2--3 weeks for serum cortisol levels and for cell depletion in thymus, spleen, femoral marrow, mesenteric, inguinal and popliteal lymph nodes. Serum cortisol peaked within 24 h and declined to normal after 4 days. Total marrow cell numbers were relatively unaffected, but in all other tissues studied, cell depletion was severe and prolonged. B lymphocytes were affected more severely than T lymphocytes. There was a transient increase in the percentage of marrow T lymphocytes but otherwise little change. The percentage of node T lymphocytes increased while that of B lymphocytes decreased. The percentage of spleen B lymphocytes was reduced severely but transiently during the period of serum cortisol elevation. Spleen T lymphocyte percentages rose steadily between the fourth and seventh days after treatment, then returned to normal. Representatives of most types of lymphoid tissue were studied. As cell losses in any one were not compensated by gains in any other, most were probably due to destruction rather than redistribution. The slow rates of recovery were also more consistent with regeneration than with reappearance after redistribution.
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PMID:Hydrocortisone and the antibody response in mice. I. Correlations between serum cortisol levels and cell numbers in thymus, spleen, marrow and lymph nodes. 51 Dec 24

We have looked at the effect of in vivo cortisone acetate treatment on effector cells for antibody-dependent cell-mediated cytotoxicity in mice and rats, using both chicken erythrocytes and the mouse lymphoma cell line AKR.A as target cells, since the AKR.A cell line is susceptible to antibody-dependent cell-mediated cytotoxicity killing only by the lymphoid effector cell, whereas a wide variety of effector cells will lyse chicken erythrocytes in the presence of antibody. The lymphoid K cell, detectable in rat spleen and blood, was unaffected by steroid treatment sufficient to cause lymphopenia, whereas splenic anti-chicken erythrocyte cytotoxicity of whole spleen and of phagocyte-free spleen was depressed in mice and rats. The greatest suppression was seen with nonphagocytic mouse spleen, and may have been in part attributable to steroid-induced redistribution of the effector cell(s), since the cytotoxic capacity of nonphagocytic bone marrow cells was increased by 70% at a time when the activity in spleen was 25% of normal.
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PMID:Effect of cortisone acetate on effector cells for antibody-mediated cytotoxicity in mouse and rat. 61 83

Inclusion of tocopherol acetate and splenin into complex treatment of viral hepatitis B (VHB) ensures a marked immunomodulating effect consisting in control of T-lymphopenia, normalization of helper-suppressor ratio, reduction of circulating immune complexes and a tendency to restoration of normal ratio between separate fractions of immune complexes, stimulation of phagocytic activity of monocytes of the peripheral blood. Splenin and tocopherol acetate are recommended in the complex treatment of hepatitis B.
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PMID:[The tocopherol acetate and splenin correction of the immunological disorders in patients with viral hepatitis B]. 144 92

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.
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PMID:Acute airsacculitis in turkeys inoculated with phorbol myristate acetate. 236 55

Subtoxic doses of endotoxin (salmonella abortus equi lipopolysaccharide, LPS) (5 micrograms/kg i.p.) or tumor necrosis factor alpha (TNF alpha) (15 micrograms/kg i.v.) induced fulminant hepatitis within 8 hr, when mice had been sensitized by a subtoxic dose of D-galactosamine (700 mg/kg i.p.). LPS-treatment led to the release of TNF into the circulation, independently of the presence of D-galactosamine. The TNF-dependent development of hepatitis was accompanied by a severe lymphopenia and neutrophilia as assessed by leukocyte differential count. The total leukocyte count was not significantly affected. Lymphopenia and neutrophilia were induced by LPS or TNF alpha alone; however, the differential count was not influenced by D-galactosamine. A quantity of 260 micrograms/kg phorbol myristate acetate (PMA) i.p. or 5 micrograms/kg platelet activating factor (PAF) i.v. or 3.3 mg/kg N-formyl-methionyl-leucyl-phenylalanine methylester (FMLP) i.v. or 167 mg/kg zymosan i.v. also caused lymphopenia and neutrophilia in mice. However, none of these agents induced the production of systemic TNF and therefore failed to induce hepatitis in D-galactosamine-sensitized mice. In LPS-insensitive C3H/HeJ mice administration of LPS produced neither differential count changes nor hepatitis while both events were observed when TNF alpha was given. This shows that TNF alpha alone gives rise to lymphopenia/neutrophilia as well as hepatitis independent of LPS. When the action of TNF alpha was blocked by anti TNF alpha antiserum pretreatment of LPS-sensitive mice, the animals were protected against LPS-induced hepatitis. However, lymphopenia and neutrophilia still occurred to a similar extent. The involvement of a putative additional mediator of LPS-induced leukocyte alterations was checked. The findings suggest that this mediator, if present, is different from IL-1, IL-2, eicosanoids or superoxide. We conclude from our findings that changes in leukocyte numbers and composition following D-galactosamine LPS or D-galactosamine/TNF alpha administration is an epiphenomenon rather than a causal event of leukocyte stimulation in the process of inducing a fulminant hepatitis in mice.
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PMID:Leukocyte alterations do not account for hepatitis induced by endotoxin or TNF alpha in galactosamine-sensitized mice. 240 85

The white blood cell (WBC) count and differential count, including the morphology and acid alpha-naphthyl acetate esterase (ANAE) activity of lymphocytes, in psoriatic patients of different types, stages, and extensiveness of skin lesions were analyzed. The number of total WBC and polymorphonuclear leukocytes was markedly increased in psoriasis erythrodermica and psoriasis pustulosa. Lymphocytopenia, especially T-lymphocytopenia, was noticed in all types of psoriasis. Antineoplastic drugs and immunosuppressants intensified the degree of T-lymphocytopenia. This might be the cause of recurrence and more recalcitrant course of the disease. Therefore, it is considered that these drugs should not be the first choice in the treatment of psoriasis.
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PMID:Peripheral leukocytes in psoriasis. 306 69

The ability of alveolar macrophages (AM) to release hydrogen peroxide (H2O2), an indicator of AM function, was studied in five children with the acquired immunodeficiency syndrome (AIDS) related complex and, for comparison, in 11 children without disorders of the lung parenchyma. In the AIDS-related complex group, pulmonary manifestations were mild, and lung involvement was suspected by moderate clinical and/or radiological features. None had a past history of opportunistic infections; neither did any have lymphopenia. Cytologic study of the bronchoalveolar lavage (BAL) fluid revealed increased cellularity with increased percentage of lymphocytes. The study of H2O2 release was performed on unstimulated AM and on AM stimulated by phorbol myristate acetate (PMA). Under both experimental conditions, the amount of H2O2 accumulated in the medium was significantly increased in the group with AIDS-related complex (P less than 0.001). As no enhanced oxidative activity has been reported in AM from patients with full-blown AIDS, an increased ability of AM to release oxygen metabolites from children with AIDS-related complex may reflect an initial and temporary step in the course of the LAV/HTLV-III pulmonary disease. Determining AM activation might be a reliable method of assessing the evolution of lung disorder in AIDS.
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PMID:Activation of alveolar macrophages from children with the acquired immunodeficiency syndrome-related complex. 323 46

Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome (SAIDS) was compared with that in age-matched normal juvenile rhesus monkeys. The functional tests were 1) chemotaxis, 2) phagocytosis of opsonized Candida albicans, 3) killing and/or growth inhibition of Candida albicans, 4) generation of respiratory burst, and 5) monocyte-derived macrophage response (morphology and/or respiratory burst) to stimulating agents such as lymphokines, gamma interferon, endotoxin, and phorbol myristate acetate. The monkeys tested had either clinical SAIDS (alive with lymphadenopathy, splenomegaly, and lymphopenia or neutropenia) or had terminal SAIDS (moribund due to the disease). Responses of monocytes from 14 monkeys with clinical SAIDS were indistinguishable from those of 9 normal juvenile rhesus monkeys, whereas monocytes from 3 monkeys with terminal SAIDS had enhanced phagocytosis and respiratory burst capacity. Chemotaxis, candidacidal/stasis activity, and response to stimulating agents were normal in these terminal cases. Plasma from the SAIDS monkeys was as capable of opsonizing yeasts and of being able to generate chemotactic factors by endotoxin as was control plasma. SAIDS retrovirus (SRV) was detected by co-cultivation of pure monocyte-derived macrophage cultures with Raji cells, an indicator cell line which forms syncytia in the presence of SRV. Four terminal SAIDS cases and one late-stage clinical SAIDS case were virus-positive when the number of macrophages in the cultures ranged from less than 50 to about 500. Terminal SAIDS monocyte-derived macrophages in culture as long as 17 days produced SRV. These data show that in monkeys with SAIDS the major effector functions of monocytes and macrophages involved in host defense are intact (even up until death). Additionally, some of the monocytes are productively infected, and these infected monocytes are viable and adherent in culture.
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PMID:Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome. 390 21

1. In mice rendered lymphocytopenic by X-irradiation or hydrocortisone acetate, pertussis vaccine evoked both lymphocytosis and polymorphonuclear leukocytosis. 2. When mice with lymphocytosis induced by pertussis vaccine were X-irradiated, prompt and extensive destruction of circulating as well as tissue small lymphocytes occurred. The devitalized circulating cells were cleared from the blood primarily by the Kupffer's cells of the hepatic sinusoids. 3. Hydrocortisone acetate administered to mice with lymphocytosis did not cause acute lymphopenia nor was there any evidence of destruction of circulating small lymphocytes. However, destruction of these cells within lymphoid tissues was apparent. These observations suggested that adrenal cortical hormones are not "lymphocytolytic" with respect to circulating lymphocytes.
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PMID:The effect of hydrocortisone and x-irradiation on the lymphocytosis induced by Bordetella pertussis. 428 58


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