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)

The objective of this investigation was to determine whether an imbalance between naive- and memory-phenotype cells occurs within CD4+ and/or CD8+ splenic T cell subsets in models of protein-energy malnutrition (PEM) which produce wasting disease (loss of approximately 1.6% of body weight per day for 14 d) and profound depression in thymus-dependent immunity. Male and female weanling mice of disparate inbred strains, CBA/J and C57BL/6J, were allocated to the following groups: zero-time control (23 d old and 19 d old, respectively), ad libitum intake of a complete purified diet (19% crude protein, 17 kJ/g gross energy), restricted intake of the complete diet, and (C57BL/6J, only) ad libitum intake of an isocaloric low protein diet (0.6% crude protein). Surface expression of isoforms of CD45, a component of the T cell receptor complex, as well as of the accessory molecule, CD2, were assessed by flow cytometry of splenic mononuclear cell suspensions. Both major T cell subsets in the malnourished groups contained a significantly higher proportion of cells expressing the surface marker, CD45RA, than was found in the spleen cells of the control groups. CD45RA+ (naive-phenotype) T cells represent the extreme of quiescence and stringent activation requirements among thymic lymphocytes. The results provide the first clear evidence of a T cell subset imbalance in PEM which is consistent with depression in acquired immunity and which occurs, apart from antigenic challenge, in a site wherein immune responses take place. The T cell receptor complex may emerge as a focal point of the depressive influence of PEM on the competence of thymic lymphocytes.
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PMID:The CD45RA+ (quiescent) cellular phenotype is overabundant relative to the CD45RA- phenotype within the involuted splenic T cell population of weanling mice subjected to wasting protein-energy malnutrition. 756 81

Bacterial superinfections are the most common cause of mortality during influenza epidemics. Depression of phagocyte functions by influenza A viruses (IAVs) is a likely contributory cause of such infections. We used an in vitro model of viral depression of neutrophil respiratory burst responses to FMLP and PMA to examine the mechanism of IAV-induced phagocyte deactivation. Respiratory burst responses or intracellular calcium mobilization were triggered by the virus itself, but these were not causally related to deactivation. By treating neutrophils with neuraminidase, and by use of purified IAV hemagglutinin (HA) preparations, cross-linking of sialic acid-bearing neutrophil surface components by the IAV HA was shown to be responsible for deactivation. IAV competed for binding to neutrophils with Abs directed against CD43, sialyl-Le(x), CD45, and gangliosides. Deactivation could be reproduced by treating neutrophils with anti-CD43 or -sialyl-Le(x) Abs in the absence of IAV. However, treatment of neutrophils with elastase markedly reduced CD43 expression, without affecting overall IAV binding or the ability of IAV to cause deactivation. Hence, although IAV binding to CD43 can account for deactivation, other IAV-binding proteins exist (e.g., those bearing sialyl-Le(x)) that can independently mediate functional depression.
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PMID:Neutrophil deactivation by influenza A virus. Role of hemagglutinin binding to specific sialic acid-bearing cellular proteins. 770 33

A single injection of pristane was given i.p. to plasmacytoma-susceptible BALB/cAn mice. At intervals up to 6 mo thereafter, immunofluorescence labeling of intranuclear terminal deoxynucleotidyl transferase (TdT), cell surface B220 glycoprotein, cytoplasmic mu-chains of IgM (c mu), and surface mu-chains (s mu), together with mitotic arrest techniques, were used to quantitate the in vivo population dynamics of precursor B cells in the bone marrow. TdT-expressing pro-B cells (TdT+B220-, TdT+B220+), before the expression of mu-chains, showed sustained increases in both population size and the number of cells flowing through mitosis per unit time. In contrast, populations of pre-B cells (c mu + s mu -) and B cells (s mu +) were consistently depressed for long periods of time, including the phase of plasmacytoma formation. Precursor B cells in DBA/2 mice, a plasmacytoma-resistant strain, showed similar responses to pristane treatment. The results demonstrate that a single injection of pristane, which greatly increases the demand for macrophage activity in the peritoneal space, causes sustained distant alterations in B cell lymphopoiesis in the bone marrow; specifically, a prolonged increased proliferation of pro-B cells coupled with a depression and a exaggerated loss of pre-B cells and B cells. The protracted stress on B cell lymphopoiesis may be a predisposing factor in the subsequent development of c-myc-activating chromosomal rearrangements that play a critical role in plasmacytomagenesis.
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PMID:Perturbation of B cell genesis in the bone marrow of pristane-treated mice. Implications for plasmacytoma induction. 786 85

This study was performed to determine whether presynaptic receptor blockade could be differentiated from postsynaptic blockade by examining the effect of increasing rates of indirect stimulation on twitch height depression (THD) on partially paralyzed in vitro rat diaphragm preparations. We calculated the T200/T1 ratio (force of the 200th stimuli divided by the force of the first stimuli) at rates of 0.2 Hz, 0.5 Hz, 1 Hz, and 2 Hz using a drug concentration which provided approximately 20% THD during stimulation at 0.1 Hz. Markedly different T200/T1 ratios were demonstrated when hexamethonium, a drug with predominantly presynaptic effects, was compared with alpha bungarotoxin, a drug with predominantly postsynaptic effects. These results were then compared with those from vecuronium, rocuronium, mivacurium, and tubocurarine. Both hexamethonium and rocuronium caused a marked decrease in T200/T1 ratio at higher rates of stimulation; alpha bungarotoxin caused a slight increase in T200/T1 ratio at higher rates of stimulation. The T200/T1 ratios produced by vecuronium, mivacurium, and tubocurarine lay intermediate between hexamethonium and alpha bungarotoxin. Significant differences in T200/T1 ratios were found when alpha bungarotoxin was compared with all other drugs at 2 Hz. Hexamethonium and rocuronium produced significant differences in T200/T1 ratio from those of all the other drugs at 1 Hz and 2 Hz. There were significant differences in the T200/T1 ratio found after hexamethonium and rocuronium compared to alpha bungarotoxin at 0.5 Hz. No significant differences at any rate of stimulation were found between hexamethonium and rocuronium. No difference was observed in the effect of vecuronium, mivacurium, and tubocurarine. We conclude that, if the observed effect is the result of hexamethonium acting predominantly at presynaptic sites and alpha bungarotoxin acting predominantly at postsynaptic sites, the relative contribution of small doses of nondepolarizing drugs at each site can be differentiated by determining the T200/T1 ratio at rates of 1 Hz or 2 Hz. Our results are consistent with the suggestion that small doses of rocuronium have marked presynaptic activity, but that vecuronium, mivacurium, and tubocurarine have both pre- and postsynaptic effects.
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PMID:The effect of rate of stimulation on force of contraction in a partially paralyzed rat phrenic nerve hemidiaphragm preparation. 908 75

The effects of orally administered sodium nitrite (20 mg NaNO2/kg b. w) on the responses of T and B lymphocytes collected from the mesenteric lymph nodes were studied in resistant AKR/J, H-2(k) haplotype mice infected with Trichinella spiralis nematode. On days 6, 9, and 12 postinfection, the mesenteric lymph node cells (MLNC) were collected from the mice and assayed for lymphocyte subsets (CD4(+), CD8(+), B220(+)), cytokines (IL-2, IL-5), and INF-gamma. At the same time, the number of adult worms in the small intestine were counted. Infection of the nitrite-treated mice with T. spiralis L1 larvae caused a marked increase in the number of adult worms in the small intestine. However, preincubation of T. spiralis L1 larvae with nitrite before infecting the mice resulted in a significant reduction in the number of adult worms (p < 0.05). Preincubation of T. spiralis L1 larvae with nitrite also caused an increase in the number of CD4(+) and CD8(+) cells as well as IL-2, IL-5, and INF-gamma levels. An increased level of CD8(+) subsets and a depression of IL-2 and IL-5 production by MLNC were observed in mice infected with larvae without nitrite pretreatment. Since supplementary rIL-1alpha was found to alter INF-gamma secretion by MLNC in vitro, the pattern of MLNC proliferation was examined further with the nitrite-treated mice. Sodium nitrite increased thymidine incorporation into the MLNC. However, INF-gamma production was not enhanced when rIL-1alpha was added to the MLNC culture obtained from nitrite-treated mice.
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PMID:Nitrite mediated T lymphocyte responses in the intestinal immune system of mice infected with Trichinella spiralis nematode. 917 17

Previous studies in critically ill patients have shown the beneficial effects of early enteral nutrition supplemented with arginine, omega-3 fatty acids and nucleotides (Impact) on immunological response, infection rate and length of stay in hospital. No specific data exist for patients with severe multiple injury, who represent a high risk group for systemic inflammatory response syndrome (SIRS), septic complications and multiple organ failure (MOF). In this prospective, randomized, double-blind controlled clinical study on patients after severe trauma (ISS ca. 40) the primary study endpoints were incidence of SIRS and MOF [definitions according to Am Soc Crit Care Med (5) and Goris (23), Sauaia (43)]. Thirty-two patients enrolled in the study, and 29 were eligible for analysis: test (Impact) (n = 16), control (n = 13). Both groups were comparable according to age, body mass index and severity of trauma (PTS-test: 38.8 +/- 12.5, PTS-control: 40.8 +/- 15.5, ISS-test: 39.6 +/- 11.4, ISS-control: 40.5 +/- 9.2). Patients were randomized to receive either Impact (test) or an isonitrogenous isocaloric diet (control). Feeding was started on the 2nd day after trauma via endoscopically placed nasoduodenal or jejunal feeding tubes. The experimental diet was safe and well tolerated. During the 1st week the enteral feeding amount was about 2000 ml without significant difference. Test-fed patients developed SIRS significantly less frequently between day 1 and day 28 (8 vs 13.3; P < 0.05) and especially between day 8 and day 14 (3 vs 6.2; P < 0.001). In the control group the Goris score was significantly worse (P < 0.05) on days 3, 4, 6, 7, 10, 11, 16 and 17 and the Sauaia score on days 8, 9, 10 and 11 (P < 0.05; P < 0.01). Mortality rate did not significantly differ (test 2/16, control 4/13), nor did length of ICU or hospital stay. With regard to the acute-phase response, C-reactive protein was significantly lower on day 4 in the test group (test: 131 +/- 67 mg/l, control: 221 +/- 110 mg/l) as was fibrinogen on day 12 (6.6 +/- 1.4 vs 7.5 +/- 1.4 g/l) and day 14 (7.1 +/- 1.3 vs 7.8 +/- 0.8 g/l). No significant difference could be observed for CD4/CD8 ratio, CD45 isotope on activated T-cells and lymphocytic interleukin (II)-2-receptor- and II-6 level. However, HLA-DR antigen presentation on peripheral monocytes was significantly elevated on day 7 in the test group (P < 0.05). According to the results, arginine, omega-3 fatty acids and nucleotides-enriched diet during early enteral feeding leads to reduction of SIRS after severe multiple injury. There is evidence for improvement of post-traumatic immunological response which helps to overcome the immunological depression after trauma.
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PMID:[Clinical effects of supplemental enteral nutrition solution in severe polytrauma]. 955 78

The causal relationship between the inhibition of antibody production and liver injury induced by single doses of acetaminophen (APAP) was investigated in mice. The liver injury and antibody production were evaluated using the serum transaminase activity and the number of antibody forming cells against sheep red blood cells (SRBC), respectively. The relevance of APAP hepatotoxicity with inhibiting antibody production was elucidated in fasted and fed mice treated with a single oral administration of APAP. In fasted mice, the oral administration of APAP produced serious liver injury, while it was not the case in the fed mice. As the antibody production was measured under these conditions, APAP significantly depressed the antibody production in fed mice as well as in fasted mice. The rate of B220 positive cells in the splenocytes was significantly decreased by APAP administration in both the fasted and fed mice. Splenocytes proliferative responses following mitogenic stimulation with concanavalin A or lipopolysaccharide were inhibited by APAP. Moreover, APAP added directly to the splenocyte culture also inhibited the in vitro antibody-producing response to SRBC. These findings indicate that the APAP-induced depression of antibody production may not be a secondary response to APAP-hepatitis, but may be a primary response to APAP.
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PMID:Inhibition of the antibody production by acetaminophen independent of liver injury in mice. 1185 66

The aim of this paper was to compare the effect of flumethasone and meloxicam in combination with oxytetracycline on clinical and immunological parameters of calves suffering from enzootic bronchopneumonia. The study was performed on 30 Black-and-White Lowland Breed calves with clinical signs of enzootic bronchopneumonia divided randomly into three equal groups and, respectively, treated with-Group I: oxytetracycline and meloxicam; Group II: oxytetracycline and flumethasone; Group III (control): oxytetracycline only. Treatment of calves with the combination of oxytetracycline and meloxicam (Group I) caused a significantly faster, in comparison to other groups, improvement in the clinical illness index score (CIIS: cough, nasal discharge, dyspnea, depression and anorexia) and a faster normalization of body temperature. A slow decrease in white blood cell (WBC) count, the number of neutrophils, MID (mixed number of monocytes, eosinophils and basophils) and in the individual number of monocytes (CD14/CD45 positive cells) was observed in Groups I and III. In the blood of the calves which received oxytetracycline and flumethasone (Group II), leukocytosis, neutrophilia and monocytosis with concomitant lymphopenia and a low number of T cells (CD2+) was observed. Moreover, the calves treated with flumethasone exhibited a decrease in gamma-globulin concentration, and phagocytic parameters. Both drugs, flumethasone and meloxicam slightly decreased tumor necrosis factor (TNF) but meloxicam slightly increased the levels of interferon (IFN) in sera and in bronchoalveolar lavages (BALs). These results suggest that the combination of meloxicam with an antibiotic in calves suffering from enzootic bronchopneumonia is superior to the antibiotic alone and also to the combination of the antibiotic with flumethasone.
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PMID:Effect of steroidal and non-steroidal anti-inflammatory drugs in combination with long-acting oxytetracycline on non-specific immunity of calves suffering from enzootic bronchopneumonia. 1451 8

Infections are among the leading causes of death in spinal cord-injured patients, and are associated with hampered wound healing, prolonged hospitalization and impaired neurological recovery. We have analysed fluctuations of immune cell populations in an experimental rat model of spinal cord injury (SCI) by FACS analysis compared with sham-operated controls to detect the responses specifically induced by SCI. Further, to illustrate the impact of SCI only animals did not receive methylprednisolone in order to exclude confounding iatrogenic factors. Experimental SCI of rats induced a depletion of ED9(+) monocytes (< 45%, P < 0.01), CD3(+) T-lymphocytes (< 35%, P < 0.01), CD45 RA(+) B-lymphocytes (< 25%, P < 0.01), MHC class II(+) (< 40%, P < 0.01) and OX-62(+) dendritic cells (< 50%, P = 0.032) within the first week after SCI. HIS 48(+) granulocytes remained on levels similar to sham-operated controls. Our data suggest that experimental SCI induces early onset of an immune suppression that we refer to as SCI-immune depression syndrome. Iatrogenic application of methylprednisolone in patients suffering may worsen the immune suppression. A deeper understanding of the underlying mechanisms of this novel syndrome might be essential to decrease mortality, costs (time of hospitalization) and to protect the intrinsic neurological recovery potential following SCI.
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PMID:Spinal cord injury-induced immune depression syndrome (SCI-IDS). 1743 62

An 11-year-old spayed-female German Shepherd dog was presented to the Veterinary Medical Teaching Hospital at Kansas State University with a history of weight loss, anorexia, depression, and lethargy for 2-3 weeks. Radiographic examination revealed a mass in the spleen and several round radiodense foci in the liver. CBC results included normocytic normochromic anemia, marked thrombocytopenia, and low numbers of neoplastic cells that frequently had cytoplasmic projections or blebs. A bone marrow aspirate contained about 80% neoplastic megakaryoblasts with the same microscopic features as those observed in peripheral blood. Using flow cytometry, cells of large size were identified in peripheral blood that expressed CD41/61, CD45, CD61, and CD62P (P-selectin) and were negative for markers of T cells, B cells, monocyte/macrophages, and dendritic cells. Because of the poor prognosis, euthanasia and subsequently necropsy were performed. On histopathologic examination, neoplastic megakaryoblasts were identified in spleen, liver, mesenteric lymph node, and the pulmonary vasculature. Using immunohistochemistry, the neoplastic megakaryoblasts weakly expressed von Willebrand factor. Based on microscopic and immunophenotypic findings, a diagnosis of acute megakaryoblastic leukemia (AMegL) was made. To our knowledge, this is the first report of AMegL in a domestic animal in which immunophenotyping by flow cytometry and a panel of antibodies against CD41/61, CD61, and CD62P were used to support the diagnosis.
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PMID:Acute megakaryoblastic leukemia in a German Shepherd dog. 1979 30


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