Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review study examined the clinical course of measles diagnosed in children being treated for malignant disease in Newcastle upon Tyne during 1973-86. Of the 17 cases diagnosed, five were fatal. Factors associated with a favourable outcome were a typical rash and Koplik's spots, which were accompanied by a detectable serum antibody response and the disappearance of measles giant cells from nasopharyngeal secretions. Pneumonitis severe enough to require assisted ventilation was invariably fatal. Pneumonitis and encephalitis were the main complications. Treatment included immunoglobulin, interferon, and ribavirin, but none could clearly be shown to be effective. The comparatively low mortality in this series may have been due to the extensive use of the fluorescent antibody technique in Newcastle during the study period and therefore detection of less severe cases as compared with other reports.
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PMID:Measles in children who have malignant disease. 311 96

After infection with the mouse pneumonitis agent (MoPn; murine Chlamydia trachomatis), heterozygous (nu/+) but not nude athymic (nu/nu) mice produced enhanced amounts of gamma interferon (IFN-gamma) in vitro in response to MoPn antigen that exhibited cytotoxic activity when added to host cells already infected with chlamydiae. Antibody-complement lysis showed the cytotoxic activity to be dependent, at least in part, on L3T4+ T cells for production. The cytotoxic responses were directed primarily against Chlamydia-infected target cells, but a second type of toxicity was demonstrable against uninfected target cells after treatment of the generating cell population with anti-Lyt-2 antibody plus complement at certain time points after infection. This additional nonspecific cytotoxic activity was presumably due to a second factor (factor X) acting in concert with IFN-gamma. Lyt-2+ cells, however, also were shown to play a role in IFN-gamma production and cytotoxicity directed against infected targets at later time points after infection. Neutralization of IFN-gamma in the samples containing cytotoxic activity abrogated the cytotoxicity against both infected and uninfected targets, but cloned murine IFN-gamma exhibited toxicity in a dose-dependent manner only against infected target cells. The data provides evidence that cytotoxicity against infected targets is due to antigen-specific induction of IFN-gamma, but other cytokine activity, most demonstrable after removal of Lyt-2.2+ cells and cytotoxic to uninfected targets, also is present.
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PMID:Gamma interferon-mediated cytotoxicity related to murine Chlamydia trachomatis infection. 313 68

In a model of pneumonia caused by murine Chlamydia trachomatis, depletion experiments with monoclonal antibody to gamma interferon (IFN-gamma) made mice more susceptible. Repletion experiments giving exogenous recombinant murine IFN-gamma were not consistently protective. IFN-gamma may be necessary but not sufficient in host defense against the organism.
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PMID:Role in vivo for gamma interferon in control of pneumonia caused by Chlamydia trachomatis in mice. 313 69

The activity of natural killers (NK) for K-562 target cells (human myeloleukemia cells) was determined in 20 patients with influenza complicated with pneumonia and in 11 patients with uncomplicated influenza. The influence of the autologous blood serum and recombinant alpha 2-interferon (reaferon) on NK activity was studied in vitro. In uncomplicated influenza, the activity of natural killers in the acute period of the disease was higher, and in patients with influenza complicated by pneumonia lower than in normal subjects. In the convalescent period, the activity of natural killers increased or approached the norm in complicated cases, and the average values showed no significant difference from those in normal subjects. The stimulating effect of the autologous blood serum and reaferon on the activity of natural killers in patients with complicated influenza was demonstrated in vitro.
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PMID:[Natural killer activity in influenza patients]. 317 29

Host defense mechanisms spaced along the respiratory tree and in the alveolar spaces effectively remove or contend with micro-organisms that enter the airways, so serious lung infections occur rarely in healthy people. Special circumstances, such as virgin exposure to a virulent microbe or a large innoculum of a pathogen, can result in illness, but usually routine surveillance host defenses are protective and suffice to keep colonizing airway flora in check. When pneumonia develops or recurrent sinopulmonary infection exists, however, some element of the normal defense apparatus may have failed or is inadequate. This review highlights several components of the apparatus, that is immunoglobulins IgG and IgA and the interaction of alveolar macrophages and lymphocytes, and examines deficiencies in their function that may result in infection. Along the conducting airways, poor mucociliary clearance and/or deficiencies in certain IgG subclass antibodies or destruction of IgA may predispose to sinopulmonary infections; these may be a manifestation of a hereditary disease. In pneumonia the alveolar macrophage is positioned as the central cell which must respond in several directions. This scavenger phagocyte first intercepts the microbe and either can kill or contain it or must call in some other phagocytic cell or inflammatory mediator(s) for assistance. Opsonic antibodies (IgG) and other nonimmune opsonins (complement and surfactant or fibronectin fragments) facilitate phagocytosis, but an absence of antibody may permit infection to develop with encapsulated bacteria (pneumococcus). Insufficient bone marrow reserves of PMNs or a paucity of chemotactic factors to attract them into the alveoli is a situation that may permit gram-negative bacilli and fungal organisms to flourish. Inability of immune T-lymphocytes to energize macrophages, through soluble cellular mediators that provide cell-mediated immunity and activation, makes containment of certain intracellular microbes impossible for these phagocytes (Legionella or mycobacteria). Likewise, concomitant infection of macrophages with viruses (human immunodeficiency virus, and cytomegalovirus or herpes viruses) plus an excessive T-lymphocyte suppressor cell influence may make P. carinii and common bacterial and fungal organisms difficult to contain in the lungs of AIDS patients. Consideration about what the lung host deficiency might be can make therapy more specific through immunization to develop special antibodies, replacement of certain immunoglobulins (IgG subclasses), or selective administration of cell mediators (gamma-interferon or interleukins).
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PMID:Host defense impairments that may lead to respiratory infections. 331 80

We investigated the effect of human recombinant DNA-derived IFN-alpha-2 given in a dose of 1-2 X 10(6) units daily by subcutaneous injection to five patients with advanced idiopathic myelofibrosis (IM). Transfusion dependent anemia and symptomatic splenomegaly were taken as inclusion criteria for this pilot study. Two patients succumbed, one and three months after starting interferon-treatment because of pneumonia and traumatic cranial injury, respectively. While on IFN-treatment no improvement of cytopenia or reduction of splenomegaly was seen in four of the patients. In one patient, however, the requirement for erythrocyte transfusions decreased from 5 to 1.7 monthly upon IFN-treatment. After two, four and six months respectively IFN-treatment had to be stopped in these cases because of progressive thrombocytopenia and/or neutropenia. These observations suggest, that IFN-alpha might be of only marginal value in the treatment of advanced idiopathic myelofibrosis.
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PMID:Interferon-alpha-2 in the treatment of idiopathic myelofibrosis. 335 3

Administration of a standard bacterial vaccine (SBV) affords some protection against influenza infection in mice if given 4 to 5 h before inoculation of the virus. This effect was enhanced by repeated injections of SBV 7 and 14 days earlier, as measured by the length of survival, mortality rate, development of gross pneumonia, and virus multiplication in the lungs. Serum interferon levels were likewise enhanced by immunization with SBV, which may, at least in part, explain the increased preventive effect.
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PMID:Enhanced effect of repeated administration of bacterial vaccine against viral respiratory infection. 435 90

Eight recipients of marrow transplants with cytomegalovirus (CMV) pneumonia diagnosed by open lung biopsy were treated with doses of human leukocyte interferon of 2 X 10(4)--6.4 X 10(5) units/kg per day to evaluate its toxicity after marrow transplant and its effectiveness against CMV infection. All eight patients died from pneumonia, and virus was still present in lung tissue from seven patients cultured after death. Interferon doses of less than or equal to 1.6 X 10(5) units/kg per day did not affect the circulating granulocyte count. Patients treated with higher doses had a decrease in circulating granulocyte count, but study of granulocyte-macrophage colony-forming cells in culture showed no evidence of toxicity to granulocyte progenitor cells. The effect on in vitro lymphocyte function was variable. Antibody production was not impaired. Interferon was not effective against established CMV infection. However, there was less hematologic toxicity than was anticipated, and the prophylactic use of interferon after marrow transplant is feasible.
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PMID:Toxicity and efficacy of human leukocyte interferon for treatment of cytomegalovirus pneumonia after marrow transplantation. 615 55

The capacity of prodigiozan to stimulate interferon production in the cell culture of the human palatine tonsil lymphocytes was studied. The interferonogenic properties of prodigiozan administered in the form of aerosols to children were also investigated. The efficacy of the prodigiozan aerosols in treatment of children with viral respiratory diseases was estimated. It was shown that prodigiozan stimulated interferon production in the cell culture of the tonsil lymphocytes (the titers of 1 : 2--1 : 8) and induced formation of endogenic interferon in the host (in the tonsils and blood serum) 24 hours after the aerosol administration. 100 micrograms of prodigiozan administered in the form of aerosols in a single dose or in 2 doses at an interval of 1--2 days had a pronounced therapeutic effect 1--2 days after the administration. The use of prodigiozan in treatment of children with acute viral respiratory infections promoted a decrease in the frequency of complications, such as pneumonia and otitis. The data are indicative of the validity of prodigiozan in treatment of children with acute respiratory infections.
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PMID:[Interferonogenic properties of prodigiozan and its effectiveness in treating acute respiratory diseases in children]. 615 58

Intraperitoneally (i.p.) injected interferon prolonged the survival time of mice inoculated intranasally (i.n.) with Sendai virus and reduced the mortality in mice inoculated i.n. with Haemophilus influenzae. Moderate concentrations of interferon were demonstrated in homogenized lungs of Sendai virus infected mice as long as the virus was present. Similar concentrations could be produced by i.p. injection of Sendai virus or interferon. Alveolar macrophages from mice treated i.p. with interferon or Sendai virus phagocytized more actively than control macropages. From the present and earlier data it is concluded that interferon may have a direct effect on the Sendai virus infection. The total effect of virus pneumonia is a reduction of the lung macrophage antimicrobial activity, and therefore the phagocytosis-modifying effect of interferon produced in the lungs is probably of minor importance for the outcome of the disease.
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PMID:Pathogenesis of Sendasi virus infection in mice. On the possible role of interferon on the development of disease. 616 Jul 24


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