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)

This study was performed to observe the therapeutic effects of interferon-gamma(IFN-gamma) and gamma-globulin(gamma-globulin) in experimental Pneumocystis carinii pneumonia of immune suppressed mice. After 9 weeks, trimethoprim-sulfamethoxazole(TMP-SMZ; 10-50 mg/mouse/day), mouse IFN-gamma(5 x 10(4) units/mouse/day) and mouse gamma-globulin(20 mg/mouse/day) were administered to the mice for 3 weeks by the experimental group. The therapeutic efficacy was evaluated by body weights, histopathologic and electron microscopic findings of the lungs, and number of P. carinii cysts by Gomori's methenamine silver stain. Body weights of the mice were significantly increased in the group of combination therapy of TMP-SMZ with IFN-gamma or gamma-globulin, and in the group of TMP-SMZ treatment (p < 0.05), however, little effect was found in the group of gamma-globulin alone. Histopathologic findings of P. carinii pneumonia were much improved in the group of combination therapy of TMP-SMZ with IFN-gamma. Treatment with either TMP-SMZ or IFN-gamma significantly reduced the number of cysts in the P. carinii pneumonia, but gamma-globulin alone was ineffective. In electron microscopic findings of P. carinii pneumonia, the number of trophozoites and cysts were reduced by treatment with either TMP-SMZ or IFN-gamma, and most of the cysts were empty or containing one or two intracystic bodies. The present results suggested, that combination therapy of TMP-SMZ with IFN-gamma had synergistic effects in treatment of P. carinii pneumonia in experimental mice.
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PMID:[Study on the therapeutic effects of interferon and gamma-globulin in experimental Pneumocystis carinii pneumonia]. 138 89

Pneumocystis carinii, and the inflammatory response it provokes, together contribute to irreversible lung damage in immunocompromised patients. P. carinii cysts were found to be capable of inducing tumor necrosis factor-alpha (TNF) release from alveolar macrophages in a concentration-dependent manner. At physiologically achievable concentrations, pentamidine isethionate (pentamidine) substantially reduces such production. Pretreatment of alveolar macrophages (AM phi) with interferon-gamma (IFN-gamma) synergizes with P. carinii to produce increased levels of TNF, a condition which pentamidine was also able to antagonize. Pentamidine treatment did not interfere with the phagocytic ability of AM phi. Considering clinical reduction of TNF could lessen P. carinii pneumonia (PCP) induced inflammation, the efficacy of pentamidine in the treatment of PCP may be partially associated with its ability to inhibit the release of inflammatory mediators such as TNF.
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PMID:Pneumocystis carinii induction of tumor necrosis factor-alpha by alveolar macrophages: modulation by pentamidine isethionate. 148 15

To study T cell and macrophage activity during measles, levels of interferon-gamma (IFN-gamma) and neopterin in plasma and cerebrospinal fluid (CSF) were measured. Plasma levels of IFN-gamma were elevated in measles (1.17 +/- 0.27) compared with healthy adults (0.13 +/- 0.06, P less than .05) and children (0.14 +/- 0.06, P less than .01). Plasma levels of neopterin were elevated in measles (32.5 +/- 2.7) compared with healthy adults (5.3 +/- 2.9, P less than .0001), healthy children (12.1 +/- 4.0, P less than .001), and children with other infectious diseases (20.6 +/- 4.0, P less than .02). IFN-gamma was increased in measles primarily during rash; neopterin remained elevated for several weeks. Levels of neopterin showed a significant positive correlation with plasma levels of soluble interleukin-2 receptor and soluble CD8, two other parameters of T cell activation. Children with measles complicated by pneumonia had higher levels of neopterin in serum than those with uncomplicated disease. Children with measles complicated by autoimmune encephalomyelitis had higher levels of neopterin in CSF than those with noninflammatory neurologic disease but lower than those with central nervous system infections. Thus, IFN-gamma seems to be produced in vivo during acute measles virus infection; deficiency of this lymphokine does not appear to correlate with increased susceptibility to secondary infections.
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PMID:Immune activation during measles: interferon-gamma and neopterin in plasma and cerebrospinal fluid in complicated and uncomplicated disease. 210 64

Interleukin-1 (IL-1), a modulatory protein with immune and inflammatory functions, is spontaneously released by tissue macrophages in lower concentrations compared with peripheral blood monocytes. Conversely, in idiopathic pulmonary fibrosis, sarcoidosis, and certain inflammatory diseases, increased amounts of IL-1 are released by alveolar macrophages (AM). We examined IL-1 production by AM from patients with adult respiratory distress syndrome (ARDS) and compared it with that in patients with severe pneumonia requiring assisted ventilation, patients with pneumonia requiring parenteral antibiotics, and healthy control subjects. In vitro, ARDS AM released significantly more total IL-1 and IL-1 beta than did ARDS AM in patients with pneumonia and in control subjects. Moreover, after stimulation of these cells with 10 micrograms/ml of lipopolysaccharide (LPS), ARDS AM significantly increased release of IL-1 and IL-1 beta. AM from patients with severe pneumonia also released greater amounts of both IL-1 and IL-1 beta as fresh explants and after LPS stimulation when compared with control subjects. Incubation of AM with 250 U/ml human interferon-gamma (gamma IFN) was associated with less IL-1 beta release. However, stimulating AM from patients with ARDS and severe pneumonia with gamma IFN plus LPS enhanced the release of IL-1 beta compared with that in patients with pneumonia and in control subjects. ARDS AM released significantly more IL-1 beta than did all of the other groups. These results demonstrate that AM from patients with ARDS are capable of releasing significantly greater amounts of IL-1, which may be related to the progression of acute lung injury.
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PMID:Elevated interleukin-1 release by human alveolar macrophages during the adult respiratory distress syndrome. 260 96

A 31-year-old patient was recurrently admitted because of pneumonia. Specialised leukocyte function tests revealed the diagnosis of an X-linked type of chronic granulomatous disease. Treatment with interferon-gamma successfully prevented new infections.
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PMID:Unexplained recurrent pneumonia: a post-childhood case of chronic granulomatous disease. 776 Sep 70

Intercellular adhesion molecule-1 (ICAM-1), a member of the immunoglobulin gene superfamily, is a cytokine-inducible adhesion molecule, which plays a central role in leukocyte migration into sites of acute or chronic inflammation. In this article we describe a sandwich immunoenzymometric method which allows rapid, semiquantitative (in "enzyme immunoassay units", EU) identification of ICAM-1 on the surface of alveolar macrophages. We evaluated this method in two groups of patients with pulmonary sarcoidosis (n = 12) or bacterial pneumonia (n = 11) and a group of healthy volunteers (n = 6), comparing the results with those obtained by immunocytochemical staining. ICAM-1 expression on the sarcoid alveolar macrophages surface was significantly elevated, as compared with control alveolar macrophages (0.76 EU +/- 0.27 vs. 0.44 EU +/- 0.12, p < 0.01). ICAM-1 expression on the surface of alveolar macrophages from patients with pneumonia was not elevated (0.48 EU +/- 0.35). Stimulation with tumour necrosis factor-alpha (TNF-alpha) or interferon-gamma (100 kU/l) led to a significant induction of ICAM-1 on the surface of control alveolar macrophages (0.76 EU +/- 0.18, p < 0.005 for TNF-alpha, 0.64 EU +/- 0.10, p < 0.005 for interferon-gamma), whereas alveolar macrophages from both patient groups did not respond to cytokines even at high dosages. ICAM-1 expression on the surface of alveolar macrophages from patients with sarcoidosis correlated with the spontaneous release of TNF-alpha by macrophages (R = 0.77, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A rapid semiautomatical enzyme linked immunoassay identifying intercellular adhesion molecule-1 (ICAM-1) on the alveolar macrophage surface. 791 44

The role of host immune responses in the pathogenesis of Legionnaires' disease is incompletely understood, due in part to the current lack of an animal model that is both susceptible to replicative Legionella pneumophila-induced lung infection and for which species-specific immunological reagents are available. We have developed a model of replicative L. pneumophila lung infection in intratracheally inoculated A/J mice. L. pneumophila was obtained in the exponential growth phase and inoculated into the trachea of 6- to 8-week-old female A/J mice. Microbiological and histopathological evidence of infection was demonstrated in mice inoculated with 10(6) colony-forming units. Development of an acute pneumonia that resembled human Legionnaires' disease coincided with exponential growth of the bacteria in the lung 24 to 48 hours after intratracheal inoculation of L. pneumophila. This was associated with increased plasma levels of interferon-gamma at 24 hours after inoculation. After 48 hours, the bacteria were gradually eliminated from the lung over the next 5 days, corresponding with resolution of the inflammatory response in the lung, thereby mimicking the outcome frequently seen in the immunocompetent human host. Treatment of animals with anti-interferon-gamma antibody enhanced bacterial replication and disease progression, indicating an important role of host immune response in resolution of the infection. Because of the availability of murine-specific reagents, this model of replicative L. pneumophila lung infection in A/J mice after intrapulmonary inoculation of L. pneumophila potentially provides an important tool for future studies investigating the role of host immune responses in the pathogenesis of Legionnaires' disease in the immunocompetent host.
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PMID:Replicative Legionella pneumophila lung infection in intratracheally inoculated A/J mice. A murine model of human Legionnaires' disease. 799 56

To evaluate the efficacy of drugs for treatment, we tried to make an animal model of Pneumocystis carinii (P. carinii) pneumonia. Specific pathogen free (SPF) rats immunosuppressed with corticosteroid were intratracheally inoculated with P. carinii. Six weeks after the inoculation, the lung sections of infected rat lung showed increased numbers of P. carinii in the alveoli and thickening of alveolar septa with mononuclear cell infiltration. From 7 to 9 weeks after inoculation, the intensity of infection became more severe, and some rats died at this period. Then, to evaluate drug efficacy in this model, we finished the drug therapy by the 6th week and used the number of P. carinii in the lung and the inflammation score as an indicator of drug efficacy. In this P. carinii pneumonia animal model, both sulfamethoxazole-trimethoprim clinically established anti P. carinii drug and interferon-gamma which is one of the lymphokines mainly produced by T lymphocytes indicated therapeutic and synergistic efficacy against P. carinii pneumonia.
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PMID:[An animal model of Pneumocystis carinii pneumonia and therapeutic efficacy of interferon-gamma in this model]. 825 17

ICR mice were infected intranasally with Mycoplasma pulmonis isolated freshly from the lungs of the rats with pneumonia. We demonstrated with high reproducibility the expressions of messenger RNAs of cytokines, tumor necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the lung tissue of M. pulmonis-infected mice. Both the viable population of M. pulmonis in the lung tissue and the titers of the neutralizing antibody in the serum increased in 7 and 14 days, respectively, and reached their maxima in 35 days after infection. Macroscopical and microscopical lesions were evident in the lungs of the mice inoculated with M. pulmonis and sacrificed in 21 days after the inoculation. Microscopically, mild infiltration of mononuclear cells and neutrophils in peribronchial and perivascular spaces were observed. The alveolar septa were swollen with infiltration of these cells. Next, mRNAs prepared from the lung tissues of M. pulmonis-infected and -uninfected mice were tested for the presence of messages specific to TNF-alpha and IFN-gamma by the reverse transcriptase-polymerase chain reaction. The expression of the genes encoding TNF-alpha and IFN-gamma was constitutively demonstrated from 24h through 35 days after the intranasal inoculation of M. pulmonis. Furthermore, cells of two types, adherent and nonadherent cells, in bronchoalveolar lavage fluids obtained from the mice 3 weeks after inoculation of M. pulmonis were found also to express the genes of TNF-alpha and IFN-gamma. These data suggest that these cytokines would play a role in both stimulation and inhibition in the development of pathological changes in mycoplasmal infection, affecting the inflammatory responses.
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PMID:[Gene expression of tumor necrosis factor-alpha and interferon-gamma in the lungs of Mycoplasma pulmonis-infected mice]. 831 7

Cytokines interleukin-2 (IL-2) and interferon-gamma (IFN-gamma) were measured from bronchoalveolar lavage (BAL) fluid and sera of 41 marrow transplant recipients and eight healthy volunteers as controls. Although IL-2 and IFN-gamma were detected in 32 and 10 patient sera respectively, IL-2 or IFN-gamma was detected in BAL of only five patients. There was no correlation of the presence of either cytokine with cytomegalovirus pneumonia, pneumonia of other etiology or absence of pneumonia. Local lung production of IL-2 and IFN-gamma as measured in BAL did not correlate with natural-killer cell activity and had no apparent role in the pathogenesis of lung disease after marrow transplant.
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PMID:Interleukin-2, interferon-gamma and natural killer cell activity in bronchoalveolar lavage fluid from marrow transplant recipients with cytomegalovirus pneumonia. 838 95


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