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)

Interleukin-5 (IL-5) acts on eosinophil differentiation and activation, suggesting the existence of a membrane receptor for IL-5 on eosinophils. Here, we report that 125I-labeled recombinant human IL-5 bound to high affinity receptors on human eosinophils, especially pulmonary eosinophils in eosinophilic pneumonia obtained bronchoalveolar lavage (BAL). No specific binding occurred on neutrophils, nor on the undifferentiated eosinophilic cell line. EoL-3, in the absence of stimulation. The specific binding of IL-5 was induced by incubation at 37 degrees C of human eosinophils and EoL-3 cells with GM-CSF and with the supernatants of BAL cells from patients with eosinophilic pneumonia. These results indicate the existence of a specific binding site for IL-5 on human eosinophils with variable affinity in eosinophil hypodense or normodense subpopulations, as previously reported for other membrane receptors. Furthermore, lung cells (BAL cells) in patients with eosinophilic pneumonia may be involved in the production certain eosinophilopoietic growth cytokines such as IL-3, GM-CSF and IL-5.
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PMID:[Characterization of a receptor for interleukin-5 on pulmonary eosinophils with eosinophilic pneumonia]. 130 41

We investigated a broad spectrum of immunoactive mediators in a mouse model of influenza. ICR mice (4-5 wk old) that were infected with a 10 LD50 dose of influenza A/PR8/34 virus died after 6 days without evidence of bacterial superinfection. Maximal virus titers were reached by day 2 postinfection, whereas the multifocal pneumonia with mononuclear cell infiltration reached its maximum at the end of infection. We measured the cytokines IL-1 alpha, IL-1 beta, IL-2, IL-3, IL-4, IL-6, IFN-gamma, TNF-alpha, granulocyte (G)/macrophage (M)-CSF, G-CSF, M-CSF, and the lipid mediators leukotriene B4 and platelet-activating factor in the cellfree bronchoalveolar lavage fluid of mice during infection. We found an early increase of IL-1 alpha, IL-1 beta, IL-6, TNF-alpha, GM-CSF, IFN-gamma, and leukotriene B4. Levels of these factors peaked between 36 h and day 3 postinfection, with the exception of IL-6 that remained at elevated levels throughout infection. G-CSF and M-CSF increased slowly and reached a maximum by day 5 postinfection. We were unable to detect IL-2, IL-3, or IL-4. PAF remained at the same level throughout infection. Our results suggest that lung-resident cells, and possibly the alveolar macrophages, participate actively in the onset of the inflammatory response against the invading virus. The inability to detect the T cell products IL-2, IL-3, and IL-4 was unexpected considering the role of T cells in the elimination of the virus in infected mice. Our observation confirms thus earlier findings about the inability of specific T cell clones to elicit an unspecific antiviral effect.
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PMID:A kinetic study of immune mediators in the lungs of mice infected with influenza A virus. 132 55

A 63-year old man with Felty's syndrome and pneumonia of unknown origin was treated with GM-CSF. Granulocyte counts increased and arthritis-related symptoms improved under GM-CSF. Pneumonia was treated effectively with antibiotics only during or after GM-CSF application. This suggests, that antibiotic-resistant infections can be treated effectively in patients with Felty's syndrome when granulocyte counts are raised by GM-CSF.
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PMID:Improvement of pneumonia and arthritis in Felty's syndrome by treatment with granulocyte-macrophage colony-stimulating factor (GM-CSF). 229 88

This paper discusses the evaluation of new macrolides and new quinolones for the treatment of Legionnaires' disease in in vitro susceptibility test, penetration to polynuclear leukocytes and treatment in an animal model. Some kinds of biological response modifier (BRMs) such as granulocyte colony stimulating factor (GCSF), monocyte CSF (M-CSF), GM-CSF, recombinant interleukin-1 (IL-1) and IL-2 were also evaluated. The antimicrobial activity (MIC) of new macrolides to Legionella pneumophila (45 strains) showed the highest activity in TE-031 (Taisho Pharmaceutical Co., Tokyo, Japan) and then rokitamycin (RKM), RU-28965 (Roussel, France), erythromycin (EM), josamycin (JM) in decreasing order of activity. According to the results of the data of cell-penetration and survival rate after treatment of guinea pigs with experimental Legionella pneumonia, the new macrolides such as TE-031, RKM and RU-28965 are expected to be more effective in the treatment of Legionnaires' disease than EM. New quinolones such as ciprofloxatin (CPFX), NY-198 (Hokuriku Pharmaceutical Co., Japan) or T-3262 (Toyama Kagaku Pharmaceutical Co., Toyama Japan) were compared to ofloxacin (OFLX), enoxacin (ENX) or rifampin (RFP) for evaluation. These drugs showed excellent activity against L. pneumophila and good penetration to polynuclear leukocytes. Regarding the treatment of guinea pig with legionella pneumonia, OFLX was the most effective, and NY-198 or T-3262 were more effective than EM treatment. The highest survival rate was obtained with IL-2 in infected guinea pigs. We also observed the efficacy of combined use of IL-2 and HR-8 10 (Horchst FRG) which is a newly developed cephem antibiotic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of severe respiratory infection. Legionella pneumonia]. 261 84

We have previously reported pulmonary eosinophils in eosinophilic pneumonia (PIE syndrome) showed two characteristics: hypodensity and nuclear hypersegmentation. Our present working hypothesis is that the eosinophil chemotactic factor and certain lymphokines may be involved in the induction of these characteristic features. Therefore, we examined whether these stimuli can induce two characteristics in vitro. Results were as follows. 1) Chemoattracts (ECF-A, histamine and PAF) can induce both nuclear hypersegmentation and hypodense eosinophils. 2) Hypodense eosinophils can be induced earlier than induction of hypersegmented nuclei (hypodense eosinophils within three hours, hypersegmented nuclei: 12 hrs). 3) Furthermore, lymphokines can not induce hypodense eosinophil. 4) However, PHA-lymphocyte culture medium (PHALCM), gamma-IFN and IL-3 + GM-CSF can induce hypersegmented nuclei but IL-2 has no effect on nuclear segmentation of eosinophils.
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PMID:Induction of hypodense eosinophils and nuclear hypersegmentation of eosinophils by various chemotactic factors and lymphokines in vitro. 264 81

An 18-year-old woman presented with coughing, fever, progressive dyspnea, and diffuse infiltrates on the chest X-ray film. Analysis of bronchoalveolar lavage fluid showed 73% eosinophils. Acute eosinophilic pneumonia was diagnosed. Methylprenisolone, 1 g per day was given for three days and her condition improved dramatically. No relapse was observed. Analysis of bronchoalveolar lavage fluid also showed lymphocytosis, abnormally high concentrations of ECP, GM-CSF, IL-5 and sICAM-1, and hypersegmentation of eosinophil nuclei. After steroid treatment almost all these findings returned to normal; only lymphocytosis remained. Precipitating antibodies against four kinds of fungi, including Trichoderma viridae, were noted in the serum, but the environmental provocation test was negative and those fungi were not detected in the environmental culture growth. Comparison of bronchoalveolar lavage findings obtained before and after steroid treatment can provide information on the mechanism of eosinophil accumulation in the lung. This case also draws attention to the relationship between acute and chronic eosinophilic pneumonia.
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PMID:[A case of acute eosinophilic pneumonia: bronchoalveolar lavage findings before and after steroid treatment]. 756

Increasing evidence suggests an important role for cytokines in the regulation of eosinophilic inflammation. In the present study we investigated the distribution of leukocytes, lymphocyte subsets, their activation state, and the cytokine profile present in BAL fluid from patients with various lung diseases associated with eosinophilia. For this purpose, we analyzed the levels of IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-8, GM-CSF, TNF-alpha, and IFN-gamma, as well as soluble IL-2 and TNF receptors, in concentrated bronchoalveolar lavage (BAL) fluid obtained from clearly defined patients with allergic and nonallergic asthma, eosinophilic pneumonia, allergic bronchopulmonary aspergillosis (ABPA), hypersensitivity pneumonitis, and idiopathic pulmonary fibrosis. BAL fluid from normal individuals and sarcoidosis patients was analyzed as noneosinophilic controls. BAL cytokine levels were compared with the cellular infiltrate and the activation state of CD4+ and CD8+ T cells as measured by the expression of IL-2 receptors (CD25), HLA-DR, and the very late activation antigen VLA-1. Beside the characteristic leukocyte infiltrate in the various lung diseases, all patients demonstrated significantly increased numbers of activated CD4 and CD8 T cells compared with normal individuals. The analysis of the cytokine profile present in BAL fluid revealed a T helper type 2 (Th2) cell cytokine pattern, with elevated IL-4 and IL-5 but normal levels of IL-2 or IFN-gamma in allergic asthma. ABPA patients demonstrated significantly increased levels of IL-4 and IL-5, with low but significantly elevated concentrations of IL-2 and IFN-gamma. In contrast, the analysis of the cytokine profile in sarcoidosis patients revealed a Th1 cell cytokine pattern characterized by increased concentrations of IL-2 and IFN-gamma but normal levels of IL-4 or IL-5. All other patient groups showed a cytokine pattern incompatible with a pure Th1 or Th2 cell response, because IL-5, IL-2, and IFN-gamma were found to be significantly increased. The BAL fluid analysis of the other, mainly non-T cell-derived cytokines and soluble receptors showed increased levels in all patients compared with normal individuals and may represent the ongoing inflammatory responses. In conclusion, whereas increased IL-4 levels were found only in diseases characterized by increased IgE production, IL-5 was elevated in all patients with increased numbers of eosinophils. The close correlation between IL-5 levels, number of eosinophils, and activated T cells further supports a role for IL-5 in causing tissue eosinophilia.
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PMID:Activated T cells and cytokines in bronchoalveolar lavages from patients with various lung diseases associated with eosinophilia. 792 34

To investigate the mechanism of eosinophilia in patients with eosinophilic pleural effusions, we measured the activities of eosinophil colony-stimulating factor (Eo-CSF) and stimulating factor for eosinophil survival in the eosinophilic pleural fluids of six patients (two with tuberculous pleuritis, two with drug allergy, and one each with chronic eosinophilic pneumonia and pleuritis associated with rheumatoid arthritis). The number of eosinophil colonies formed by the pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of control patients with noneosinophilic pleural effusions (7.5 +/- 1.9 colonies/10(5) bone marrow cells, n = 6, versus 0.3 +/- 0.1 colonies/10(5) bone marrow cells, n = 6, P < 0.01). Similarly, eosinophil survival evaluated on day 4 of culture with pleural fluid of patients with eosinophilic pleural effusions significantly exceeded that of patients with noneosinophilic pleural effusions (83.9 +/- 9.8% versus 46.1 +/- 11.2%, P < 0.001). Both activities were inhibited mainly by anti-IL-5 antibody and partially by anti-GM-CSF antibody and anti-IL-3 antibody. Mononuclear cells obtained from eosinophilic pleural fluid released the activities of Eo-CSF and stimulating factor for eosinophil survival in vitro. These findings suggest that GM-CSF, IL-5, and IL-3 are important to eosinophil accumulation in pleural cavity as stimulators of proliferation and survival of eosinophils.
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PMID:Factors that stimulate the proliferation and survival of eosinophils in eosinophilic pleural effusion: relationship to granulocyte/macrophage colony-stimulating factor, interleukin-5, and interleukin-3. 832 45

Use of growth factors to augment hematopoietic recovery after cytotoxic therapy is a useful method for dose intensification. We wanted to evaluate the clinical and cost-effectiveness of granulocyte-macrophage colony stimulating factor (GM-CSF; Leucomax) in patients undergoing autologous bone marrow transplantation (ABMT) for Hodgkin's disease. Twenty-four patients with Hodgkin's disease were treated with high-dose chemotherapy and ABMT. Patients were then randomized in a double-blind manner to receive GM-CSF intravenously (10 micrograms/kg) over 6 h or placebo until the absolute neutrophil count (ANC) was greater than 1000/mm3 for 3 days. The study medication was stopped after 30 days. Patients treated with GM-CSF (n = 12) had shorter periods of neutropenia (median duration of an ANC of less than 1000 cells/mm3, 16 versus 27 days on placebo; p = 0.23), shorter periods of platelet-transfusion dependency (median duration, 13.5 versus 21 days on placebo; p = 0.03), shorter hospitalizations (median hospital stay, 32 versus 40.5 days on placebo; p = 0.0004). Other clinical outcomes, such as frequency and severity of toxicities, development of pneumonia or infection, in-hospital death, and response rate were similar in the two groups. Actuarial long-term disease free survival was 58% for patients treated with GM-CSF and 50% for patients who received placebo after 38 months of follow up (p = 0.6).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of granulocyte-macrophage colony stimulating factor (GM-CSF) after autologous bone marrow transplantation for Hodgkin's disease. 834 51

Recombinant human (rh) granulocyte-macrophage colony-stimulating factor (GM-SCF) is currently being tested in clinical trials for the treatment of acute myeloid leukemias with two main intentions: reduction of neutropenia and recruitment of leukemic blasts into cell cycle to enhance cytarabine (ara-C) mediated cytotoxicity. We report a case of a fatal spleen rupture in a patient with acute monocytic leukemia (AML M5b) who was treated according to a clinical phase I/II protocol with rh GM-CSF priming and standard induction chemotherapy TAD 9 (thioguanine/ara-C/daunorubicin). During treatment we observed rapidly rising peripheral blast counts and the development of an acute abdomen. Ultrasound examination revealed splenomegaly due to diffuse cellular infiltration and spleen rupture. The patient died 17 days later due to pneumonia and renewed spleen hemorrhage. Bone marrow progenitor assays before treatment showed exclusive growth of monocytoid blast cell colonies (CFU-L). Colony growth could be stimulated with rh GM-CSF and blocked dose-dependently by a monoclonal anti-GM-CSF antibody. CFU-L proliferation also increased after stimulation with rh interleukin-3 (rh IL-3) and supra-additively with rh granulocyte colony-stimulating factor (rh G-CSF) combined with rh GM-CSF. Furthermore, rh GM-CSF induced surface marker expression of CDw 65 and CD 11b on isolated CFU-L blasts. After short-term suspension culture, rh GM-CSF enhanced the expression of CD 29- and CD 11b-adhesion molecules on peripheral blast cells. In summary, this case represents a fatal spleen rupture occurring during rh GM-CSF priming and induction chemotherapy for acute monocytic leukemia. Although the etiology of this spleen rupture remains uncertain, in view of our data we suggest special caution, when further testing this therapy protocol in acute leukemias with monocytic subtype and high peripheral blast cell counts.
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PMID:Fatal spleen rupture during induction chemotherapy with rh GM-CSF priming for acute monocytic leukemia. Clinical case report and in vitro studies. 845 Jun 76


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