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

The antigen, CD69, has been demonstrated to be expressed on activated T cells and natural killer cells. There have been no studies concerning the expression of CD69 on eosinophils. In this article, we demonstrate that lung eosinophils obtained from the bronchoalveolar lavage fluid of patients with eosinophilic pneumonia expressed significant levels of CD69, whereas peripheral blood (PB) eosinophils did not express CD69. We also activated PB eosinophils in vitro using phorbol myristate acetate and cytokines to determine whether CD69 was expressed. PB eosinophils expressed CD69 after short-term culture with phorbol myristate acetate and eosinophil hemopoietic cytokines (interleukin-3, granulocyte-macrophage--colony-stimulating factor, and interleukin-5). These findings suggest that CD69 may be a useful marker for activated eosinophils at inflammatory sites.
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PMID:In vivo expression of CD69 on lung eosinophils in eosinophilic pneumonia: CD69 as a possible activation marker for eosinophils. 150 Jun 24

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

We describe the clinical features, eosinophil surface analysis, and concentration of interleukin-5 (IL-5) in bronchoalveolar lavage (BAL) and in peripheral blood (PB) of a young male patient with acute eosinophilic pneumonia. Eosinophilic pneumonia was diagnosed by BAL and by its clinical course. There was no evidence of an infectious etiology, and the patient showed rapid improvement with methylprednisolone pulse therapy (1 gm/d for 3 d). Significant differences in the expression of surface molecules such as CD54, HLA-DR, and CD69 were observed between BAL and PB eosinophils; IL-5 concentrations in BAL and in PB before treatment were 450 pg/ml and 700 pg/ml, respectively. After treatment, IL-5 concentration in PB was reduced to below 100 pg/ml. The patient has shown no recurrence after treatment.
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PMID:Adhesion molecules on eosinophils in acute eosinophilic pneumonia. 769 63

We describe an acute eosinophilic pneumonia (AEP) patient with bronchoalveolar lavage fluid (BALF). Eosinophil cell number (47%), content of interleukin (IL)-5 (8.22 x 10(2) pg/ml) and eosinophil cationic protein (9.25 micrograms/ml) were high in BALF. No eosinophilia was seen in peripheral blood on admission; however, content of IL-5 was 9.47 x 10(2) pg/ml. After methylprednisolone pulse therapy, he improved rapidly with a reduction in eosinophil cell number (7%) and the content of IL-5 (< 100 pg/ml) in BALF. However, a high content of IL-5 (6.9 x 10(2) pg/ml) and transient eosinophilia (17.5%) were seen in peripheral blood. It is important to distinguish between AEP and infectious pneumonia, because of the differing treatments. If the diagnosis of AEP is doubtful, BALF should be performed early.
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PMID:IL-5 predominant in bronchoalveolar lavage fluid and peripheral blood in a patient with acute eosinophilic pneumonia. 771 86

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

Cytokine production has been assessed at the single-cell level (ELISPOT assay) for freshly isolated mediastinal lymph node cells from C57BL/6 mice with primary, nonfatal influenza pneumonia. The mediastinal lymph node populations were also secondarily stimulated in vitro, and culture supernatants were assayed by enzyme-linked immunosorbent assay. Both approaches showed minimal evidence of protein secretion for interleukin-4 (IL-4), IL-5, and tumor necrosis factor, while IL-2, IL-10, and gamma interferon (IFN-gamma) were prominent throughout the response. The numbers of IL-2- and IFN-gamma-producing cells were maximal at 7 days after infection, while the total counts for cells secreting IL-10 were fairly constant from day 3 to 7. The cultures that were stimulated with virus in vitro showed in inverse relationship between IL-10 and IFN-gamma production, with IL-10 peaking on day 3 and IFN-gamma peaking on day 7. Lymphocytes secreting IL-2, IL-10, and/or IFN-gamma were present in CD4+ and CD8+ populations separated by fluorescence-activated cell sorting, although the CD8+ T cells produced less cytokine and were at a relatively lower frequency. Addition of recombinant IL-10 to the virus-stimulated cultures decreased the amount of IFN-gamma that could be detected, while incorporation of a monoclonal antibody to IL-10 had the opposite effect. A neutralization experiment also indicated that IL-2 was the principal mediator of lymphocyte proliferation. These experiments thus show that the developing T-cell response in the regional lymph nodes of mice with influenza cannot be rigidly categorized on the basis of a TH1 or TH2 phenotype and suggest possible regulatory mechanisms.
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PMID:Concurrent production of interleukin-2, interleukin-10, and gamma interferon in the regional lymph nodes of mice with influenza pneumonia. 815 76

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

Chronic eosinophilic pneumonitis (CEP) is characterized by longstanding respiratory symptoms accompanied by a massive pulmonary eosinophil infiltration. We hypothesized that cytokine(s) produced in the disease sites are implicated in the pathophysiology of CEP. We studied peripheral blood and bronchoalveolar lavage fluids (BALF) obtained from two lung segments of a patient with CEP. Seventy times more eosinophils were found in the BALF from an involved lung segment (showing patchy opacification on a chest roentgenogram) than from an uninvolved segment. The eosinophil-active cytokines interleukin-5 (IL-5), IL-6, and IL-10 were strikingly elevated in the BALF from the involved lung segment, whereas no or minimal levels of these cytokines were detectable in the BALF from the uninvolved segment or serum, respectively. Leukocytes in the involved lung segment, but not those in peripheral blood, expressed messenger ribonucleic acid (mRNA) for IL-5, IL-6, and IL-10. In contrast, IL-2, IL-3, IL-4, interferon-gamma (IFN-gamma), granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha (TNF-alpha) were not detected in any sample. These findings suggest that increased production of several cytokines, such as IL-5, IL-6, and IL-10, in the involved lung segment, but not in the uninvolved lung segment or peripheral blood, is a critical pathophysiologic feature of CEP.
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PMID:Cytokine production at the site of disease in chronic eosinophilic pneumonitis. 861 78

A 73-year-old man developed organized pneumonia with severe right-sided eosinophilic pleural effusion (PE). CD69+ and HLA-DR+ eosinophils in PE were 90 and 31%, respectively, but were undetectable in peripheral blood (PB). CD4+, CD45RA+ (naive) and CD4+, CD45RO+ (memory) cells in PB, PE and bronchoalveolar lavage (BAL) were 10.9, 8.4, 2.5 and 22.7, 38.3 and 16.4%, respectively. CD8+, CD45RA+ (naive) and CD8+, CD45RO+ (memory) cells in PB, PE and BAL were 3.5, 4.7, 1.0, and 8.9, 11.3 and 46.0%, respectively. The concentrations of interleukin-5 (IL-5) and IL-6 in PE were 1,680 and 2,797 pg/ml, respectively; however, these cytokines were undetectable in PB. The patient died 1 month after surgery to remove right thickened pleura. Microscopic findings showed right fibrinous pleuritis and organized pneumonia.
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PMID:Immunological analysis of organized pneumonia with eosinophilic pleural effusion. 885 30


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