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)

Alpha- and gamma-interferon (IFN) production by peripheral blood mononuclear cells (PBMC) from 18 patients affected by primary immunodeficiency syndromes was examined and compared with that of 20 normal donors. Patients included 8 with common variable immunodeficiency (CVI), 2 with congenital agammaglobulinemia, 4 with ataxia-telangiectasia, 2 with hyper-IgE syndrome, 1 with chronic EBV infection, 1 with combined immunodeficiency, and 1 with immunodeficiency with hyper-IgM. No spontaneous IFN production was observed in either patients and controls. Newcastle disease virus-induced alpha-IFN production was found to be normal in all patients. Gamma-IFN was induced by both galactose oxidase and staphylococcal enterotoxin (B). Gamma-interferon production was low or undetectable in patients with ataxia-telangiectasia, in immunodeficiency with hyper-IgM, and in hyper-IgE syndrome. No major defect of gamma-IFN was found in other types of immunodeficiency, despite the presence of occasional low producers (1 of 8 CVI patients and 1 case of congenital agammaglobulinemia). No correlation was found between IFN production and natural killer activity in individual patients. The analysis of lymphocyte subsets by monoclonal antibodies revealed gross imbalances of helper/inducer and suppressor/cytotoxic subpopulations, but no overall correlation could be established with gamma-IFN production. The observation of major defects in gamma-IFN yield only in diseases with depression of T cell-mediated immunity might contribute to a better understanding of the pathogenetical mechanisms in these diseases. Moreover, future studies should monitor these in vitro functions and their modifications by in vitro or in vivo manipulations.
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PMID:Interferon production in primary immunodeficiencies. 609 14

In mice treated with ordinarily sublethal doses of parathion 2 to 5 days postinfection with murine cytomegalovirus (MCMV) 50 to 100% mortality was observed. These mortalities appeared to be due to a decrease in the ability of infected mice to detoxify parathion. Pentobarbital-induced sleeping time was also enhanced 3 and 6 days postinfection and cytochrome P-450 concentrations were markedly depressed in mice tested 3 days after infection. MCMV-induced effects on sensitivity to parathion and pentobarbital did not appear to be directly attributable to liver infection since concentrations of virus in the liver persisted at maximum concentrations well beyond the time when sensitivity to these compounds returned to normal. The time frame during which enhanced sensitivity to parathion and pentobarbital was observed suggests that this sensitivity may have been caused by viral-induced interferon-mediated depression of cytochrome P-450.
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PMID:Increased susceptibility to parathion poisoning following murine cytomegalovirus infection. 609 89

Effector mechanisms responsible for protection against ectromelia virus (EMV) including antiviral activity of non-immune macrophages, cytotoxic T cells, antiviral antibody, delayed footpad reaction to viral antigen and interferon induction after viral infection were depressed in BALB/c mice bearing syngeneic Meth A tumors. The degree of viral growth correlated well with the depression of delayed footpad reaction, antibody production and interferon induction. But a control level of these elements could be obtained by pretreatment of tumor-bearing mice, with PSK Cytotoxic activity may not be the principal effector, since cytotoxicity was induced in both normal and tumor-bearing mice to almost the same extent but an explosive viral growth was observed only in the latter. These results suggest that PSK was responsible for restoring the depressed antiviral protective immunity to normal levels in tumor-bearing animals.
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PMID:[Depression of protective mechanisms against ectromelia virus infection in tumor-bearing mice and its prevention by PSK]. 609 65

1. Rainbow trout, Salmo gairdneri, produce elevated amounts of a serum acute phase (C-reactive) protein (CRP) when administered a variety of chemicals of environmental importance. 2. Compounds administered in doses which induce the cytochrome(s) P450 catalytic enzymes in trout hepatic microsomes also induce serum CRP. 3. However, an interferon-inducing virus does not induce CRP. Interferon induction by the virus is not significantly inhibited by chemicals which induce trout cytochrome(s) P450. 4. Simultaneous administration of chemicals and virus or virus alone results in depression of P450 protein production and only minor induction of CRP. 5. Thus, as with mammals, a reciprocating relationship appears to exist between the hemeprotein monooxygenase and immune systems of this freshwater teleost, and C-reactive protein appears to fit the reciprocating scheme closer to the cytochromes P450 response.
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PMID:Induction in rainbow trout of an acute phase (C-reactive) protein by chemicals of environmental concern. 613 74

Induction of type II interferon by sensitization of mice with Mycobacterium tuberculosis strain BCG and challenge with tuberculin resulted in a depression of the cytochrome P-450 drug metabolism system of the liver. The degree of depression was significantly greater than in mice that were only sensitized to BCG. Cytochrome b5 levels were not affected. In addition, the level of the depression of the cytochrome P-450 system correlated with the levels of type II interferon induced. Passive transfer of exogenous type II interferon preparations also significantly depressed the cytochrome P-450 system. Passive transfer of mock interferon or of normal serum had no effect.
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PMID:Type II interferon induction and passive transfer depress the murine cytochrome P-450 drug metabolism system. 615 62

The ability of polyriboinosionic acid [poly(rI)].polyribocytidylic acid [poly(rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) complexed with poly L-lysine and carboxymethylcellulose [poly(ICLc)] to induce interferon and the comparative toxicity of each in cats were evaluated. Each induced high levels of circulating interferon, although poly(ICLC) injected intravenously at 1 to 4 mg/kg induced up to 10 times more interferon than the other compounds. Each compound was pyrogenic and caused a transient decrease in leukocyte numbers. Poly(rI).poly(rC) and the mismatched analog caused severe diarrhea and nausea at the highest drug concentrations (1 to 4 mg/kg), but poly (ICLC) did not. Each compound also caused depression and lethargy and impaired coordination.
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PMID:Interferon induction by and toxicity of polyriboinosinic acid [poly(rI)].polyribocytidylic acid [poly (rC)], mismatched analog poly (rI).poly[r(C12Uracil)n], and poly(rI).poly(rC) L-lysine complexed with carboxymethylcellulose. 615 63

Susceptibility of eight strains of influenza A and B viruses to interferon and to poly(I) . poly(C) were determined by the plaque reduction method. All strains tested were slightly less susceptible than vesicular stomatitis virus (VSV) in an established line of canine kidney (MDCK) cells. The 50% plaque depression doses (PD50) of poly(I) . poly(C) for influenza A and B viruses were as high as 3.0- to 4.5-fold and 6- to 18-fold that for VSV, respectively. The amounts of interferon required to inhibit plaque formation of influenza A and B viruses by 50% were 3.0-6.2 and 7.3-15.2 units/ml, respectively. The ratio of PD50 of poly(I) . poly(C) for each strain of influenza viruses tested to that for VSV in chick embryo cells was almost the same as in MDCK cells. Furthermore, in chick embryo cells, the strains of influenza virus tested were demonstrated to be much more susceptible to poly(I) . poly(C) than both Newcastle disease virus and vaccinia virus. It is suggested that influenza viruses may be relatively susceptible to interferon and to poly(I) . poly(C).
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PMID:Susceptibility of influenza viruses to interferon and to poly(I) . Poly(C) determined by the plaque reduction method. 615 60

The influence of herpes zoster virus infection on cell-mediated and humoral immunity to varicella-zoster virus (VZV), cytomegalovirus, and herpes simplex virus (HSV) was followed in 17 zoster patients from the first week to 6 months after start of eruptions. The clinical responses were registered and correlated to the immune responses. A significant depression in blast transformation on stimulation of lymphocytes with all three antigens was found on days 1 to 5 compared with transformations later after zoster eruptions and compared with controls. Phytohemagglutinin exhibited the same stimulation in the different groups and controls. No significant differences in interferon production in the various groups and controls were found on stimulation with the VZV and HSV antigens. All zoster patients became seropositive by complement fixation to VZV a few days after start of the zoster eruption. Two zoster patients showed a fourfold rise in complement fixation antibodies to HSV. Three patients had changes in complement fixation titers to cytomegalovirus, which could indicate new infection or reactivation of infection with this virus. A significant lower transformation index to VZV was found during the first 9 days in zoster patients with fever compared with patients without fever. The relevance of this observation is discussed in relation to a previous similar observation from our group.
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PMID:Cell-mediated and humoral immunity to herpesviruses during and after herpes zoster infections. 616 9

The effects of interferon inducers on different cytolytic mechanisms were studied in the high leukemia mouse strain AKR. A clear depression in baseline cytolytic potential and interferon-mediated stimulation of natural killer cell activities was demonstrated. This depression was most pronounced after 8 weeks of age. In contrast, antibody-dependent, cell-mediated cytotoxicity against IgG-coated chicken red blood cells was always normal. Bone marrow chimeras between CBA and AKR mice were produced to investigate the influence of bone marrow vs. host-mediated factors in these two strains with regard to interferon induction and cytolytic functions. Bone marrow genotype was found to be the dominating factor with regard to both parameters. Mice reconstituted with AKR bone marrow were deficient both in interferon production using tilorone and Newcastle disease virus as inducers, and at the level of natural killer cells responding to exogenously administered interferon. The possible relationship between these findings and the development of lymphomas in AKR mice is discussed.
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PMID:Variation of interferon induction at the bone marrow level. Studies on interferon induction in relation to natural cell-mediated cytotoxic mechanisms. 617 33

This study investigated the defective natural killer (NK) cell activity in two patients with the Chediak-Higashi syndrome (CHS) using both a standard 51-chromium release microcytoxicity and a single cell-in-agarose assay against K562 and Molt-4 target cells. CHS patients were deficient in overall maximum NK capacity, but had normal percentages of potentially cytotoxic target bindng cells. the relative number of TBC that could kill bound targets (i.e., "active" NK cells) was significantly depressed in CHS patients when compared with normal controls. The diminished CHS active NK cells that were present, however, were capable of recycling and lysing multiple target cells during the assay period. In vitro interferon (INF) treatment of normal and CHS effector cells did not alter target cell binding, but did increase the maximum NK capacity, percentage of active NK cells and the maximum recycling capacity, as well as the rate of lysis. These studies indicate that the depression of NK activity in patients with CHS is secondary to a deficiency of active NK cells. The CHS active NK cells that are present, however, are capable of normal target lysis and recycling. Potentially cytotoxic pre-NK cells, which can bind but not kill target cells, can be activated by in vitro IFN to develop lytic activity. Thus, IFN treatment may be of potential benefit to the immune surveillance network of CHS patients by activating a population of pre-NK cells to express their cytotoxic potential.
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PMID:Deficiency of active natural killer cells in the Chediak-Higashi syndrome. Localization of the defect using a single cell cytotoxicity assay. 617 15


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