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)

To better define the mechanisms by which viruses depress immune function, the effect of influenza infection on the ability of macrophages to accumulate at sites of inflammation was determined. Mice were inoculated with virus, and their inflammatory response measured in vivo by counting the number of leukocytes which accumulated in the peritoneal cavity 2 days after an intraperitoneal injection of phytohemagglutinin. Mice infected with influenza had a 57% and 65% depression of total leukocyte and macrophage accumulation, respectively, as compared to the response of uninfected mice. In contrast, bacterial pneumonia did not produce a decrease in the macrophage response. This indicated that the depression was produced by the virus infection rather than being a nonspecific phenomenon accompanying any inflammatory focus in the lung. The in vitro chemotactic responsiveness of normal peritoneal macrophages incubated with infectious influenza virus was 53% of normal. These experiments suggest that influenza infection may depress a host's ability to mobilize macrophages to inflammatory sites in vivo by inhibiting their chemotactic responsiveness.
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PMID:Effect of virus infection on the inflammatory response. Depression of macrophage accumulation in influenza-infected mice. 1 95

Model systems of respiratory infection in mice were established with Streptococcus pneumoniae, influenza virus, and Mycoplasma pulmonis. The LT50 for S. pneumoniae was 2 1/2 days, for lethal influenza 6 days, and for M. pulmonis 5 days. Morbidity in sublethal influenza infections reached a peak during days 5 to 10, with recovery indicated by the third week. The course of each pulmonary infection was followed by use of the animal's maximal ability to consume oxygen (VO2max by determining the weight, compliance, and stability of the excised lung, and in some cases by following O2 consumption of minced tissue. Depression of VO2max began early in each infection; reductions ranged from 9% at the peak of sublethal influenza infection to 50% 12 to 48 hr before the LT50 of fatal infections. The depressions were not relieved by 100% O2. The noninvasive VO2max test, evoked by cold air, was simple, rapid, and reproducible and appeared to serve as a quantitative measure of over-all function during infection. Each type of infection caused an increase in lung weight, with the largest noted during fatal Mycoplasma illness and lethal influenza. The effects on lungs by influenza and M. pulmonis infections were similar but could be differentiated from those with S. pneumoniae. With sublethal influenza, CL was reduced 30% between days 5 to 10, with recovery by the third week. Ctis was not affected. M. pulmonis infections and lethal influenza caused depressions in CL of over 60% by day 4 but only a 30% decrease in Ctis. The data suggest that the decreased compliance in influenza and M. pulmonis infections was due primarily to increased surface tension. In contrast, S. pneumoniae did not affect compliance.
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PMID:Oxygen uptake and lung function in mice infected with Streptococcus pneumoniae, influenza virus, or Mycoplasma pulmonis. 2 1

The chemotactic responsiveness of monocytes from patients with serologically proven influenza infection has been quantified in vitro. Individuals with acute influenza had a significant (P less than 0-001) depression of monocyte chemotaxis. The depression ranged from 40% to 72% during acute infection but rose to normal by three weeks after recovery. When isolated mononuclear leucocytes from the recovered patients were incubated with the infecting strain of virus (Port Chalmers), a 49-54% inhibition of chemotaxis was obtained. These findings support the hypothesis that the altered immune responsiveness and increased predisposition to superinfections found frequently in patients with influenza can be due to the ability of the virus to depress monocyte function.
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PMID:Depressed monocyte chemotaxis during acute influenza infection. 5 52

Cell-mediated immune responses were examined in 19 normal volunteers after intranasal administration of three strains of influenza A virus. Eight volunteers manifested respiratory tract illness along with fourfold rises of serum antibody and/or virus shedding. Samples of peripheral venous blood were obtained before and two days, five days, and four weeks after challenge. During acute illness, infected volunteers showed lymphopenia, which persisted for up to four weeks after challenge. The lymphopenia involved thymus-derived, bone marrow-derived, and null cells. Blastogenic responses of lymphocytes to stimulation with phytohemagglutinin, concanavalin A, and streptokinase-streptodornase were depressed during acute illness, and responses to phytohemagglutinin and concanavalin A remained depressed at four weeks after infection. Thus, influenza infection in humans can result in prolonged depression of numbers and functions of circulating lymphocytes.
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PMID:Cell-mediated immune responses in humans after induced infection with influenza A virus. 30 Jul 61

A model of salicylate intoxication was developed in ferrets to permit the evaluation of the interaction with viruses isolated from patients with Reye's syndrome. Salicylate intoxication produced a mild elevation of the serum glutamic oxaloacetic transaminase and fatty changes in the liver, but these changes differed from those seen in Reye's syndrome on light and electron microscopy. Salicylates were associated with decreased activity of hepatic phosphorylase and a slight depression of activity or ornithine transcarbamylase, a mitochondrial urea cycle enzyme. Infection with influenza viruses produced mild fatty changes in the liver, but did not significantly potentiate the effects of salicylate intoxication on the over-all mortality, the degree of fatty changes, or the hepatic enzymes. Influenza infection alone was not associated with decreased hepatic phosphorylase activity, but was associated with decreased activity of ornithine transcarbamylase. Influenza A was isolated from the livers of two of four animals cultured in embryonated eggs.
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PMID:Salicylate intoxication and influenza in ferrets. 43 1

Bivalent influenza vaccine (containing antigens A/Victoria and A/New Jersey) was administered to 52 patients with hematologic malignancies, and pre- and postvaccination antibody titers to both antigens were determined by hemagglutination-inhibition. In comparison to healthy controls, mean antibody titer elevations were lower for both antigens in all disease groups, being significant (p less than 0.05) for A/Victoria in patients with non-Hodgkin's lymphoma, acute leukemia and lymphoproliferative diseases, and for A/New Jersey in patients with Hodgkin's and non-Hodgkin's lymphomas. In comparison to controls, significant depression of antibody response to both antigens was seen in patients on combination chemotherapy (p less than 0.0005), to a lesser extent in patients on daily single alkylating agent chemotherapy (p less than 0.05), while untreated patients did not differ significantly. Lymphopenia and depressed immunoglobulin levels were associated with a higher failure rate in eliciting "protective" greater than or equal to fourfold antibody titer increases. The findings suggest that patients with hematologic malignancies who are receiving chemotherapy at the time of vaccination are unlikely to attain seroconversion to protective antibody levels with influenza vaccine.
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PMID:The influence of chemotherapy on response of patients with hematologic malignancies to influenza vaccine. 76 Nov 65

Studies of the immunogenicity of red blood cells (RBC) modified by interaction with viral agents show that measles hemagglutinin or adsorption-elution of influenza virus are able to induce modifications in the RBC immunogenicity, consisting in a depression of antibody synthesis and in a stimulation of the cell-mediated immune response. The modifications depend on the extent to which RBC-surface-bound viral antigens would mask the erythrocyte antigenic determinants.
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PMID:Virus-induced modifications in the immunogenicity of red blood cells. 81 6

Cell-mediated immunity (CMI) was assessed during infection and after convalescence in 12 patients with influenza pneumonia and 10 patients with bacterial pneumonia. The patients with influenza pneumonia had a marked impairment of skin test reactivity, and their lymphocytes showed a diminished response to phytohemagglutinin and streptokinase-streptodornase stimulation in vitro. Suppression of CMI was related to the severity of the pneumonia. Patients with bacterial pneumonia showed as great a suppression of the response to phytohemagglutinin and streptokinase-streptodornase as the patients with viral pneumonia. All parameters of CMI returned to normal in both groups after convalescence. The depression of CMI could not be related to a decrease in the number of thymus-derived lymphocytes or to serum-suppressive factors in these patients.
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PMID:Effect of viral and bacterial pneumonias on cell-mediated immunity in humans. 108 45

Eighteen volunteers in tow study groups were inoculated with influenza A (H3N2) and their peripheral blood T, B and null cells enumerated at subsequent intervals. Infection with wild-type virus or with a live, attenuated virus vaccine markedly reduced the proportion and absolute number of T-cell rosettes 24 hours after inoculation. T-Cell depression preceded the onset of clinical illness in symptomatic subjects, continued during illness, and returned to normal with recovery. T-cell lymphopenia was most pronounced in volunteers infected with wild-type virus and was accompanied by an increase in null cells. Lymphocytes from six wild-virus recipients with T-cell leukopenia were incubated in vitro with a calfthymus extract (thymosin), significantly increasing the percentage of T rosettes in all six subjects (P less than 0.0001). These data indicate that influenza is accompanied by pronounced quantitative and functional changes in T cells.
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PMID:Influenza: response of T-cell lymphopenia to thymosin. 108 84

Relationship between depression of early protection against influenza virus infection and the decrease in the number of peripheral polymorphonuclear leukocytes in cyclophosphamide-treated mice was investigated using protein-bound polysaccharide (PSK), which had been shown to exert a potent restorative effect on leukocytopenia in immunocompromised hosts. Following intranasal inoculation with influenza virus (1.5 x 10(3) PFU) into untreated mice, the pulmonary virus titer progressively increased during 3 days and decreased gradually from the day 7 after infection. The treatment of mice with cyclophosphamide (150 mg/kg) 2 days before infection markedly enhanced the pulmonary virus multiplication from the early phase of infection, and the higher virus titer was maintained thereafter. When mice were given cyclophosphamide after PSK-treatment, virus titers from the early to late phases of infection were lower than those in untreated mice.
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PMID:Depression of early protection against influenza virus infection by cyclophosphamide and its restoration by protein-bound polysaccharide. 133 97


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