UMLS:C0032285 - FACTA Search

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Query: UMLS:C0032285 (pneumonia)
54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute eosinophilic pneumonia (AEP) is a recently described illness and the number of case reports has increased during the last few years. However, the role of interleukin (IL)-5 and activated lymphocytes in the pathogenesis or activity of AEP is still not clear. The clinical features, lymphocyte surface analysis and IL-5 concentrations in bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) of a young female patient with AEP are described before and at 2 weeks, 4 weeks and 6 months after a 3-day course of i.v. methylprednisolone. Serum and BALF concentrations of IL-5 before treatment were 5,200 and 8,400 pg x mL(-1), respectively. Activated CD4 lymphocytes bearing CD25 and human leukocyte antigen (HLA)-DR in BALF were higher than in PB. Treatment caused a rapid fall in these cells and levels of IL-5 in BALF returned to normal levels in parallel with clinical improvement. There was no evidence of recurrence after cessation of steroid therapy. In contrast, eosinophilia in BALF persisted for 4 weeks after steroid therapy in spite of normalization of the chest radiograph and arterial blood gases. The number of CD8+CD11b- (suppressor/cytotoxic) T-cells subsequently increased while the number of CD8+CD11b+ cells decreased. These results suggest that activated CD4 cells and interleukin-5 elevation contribute to the development of acute eosinophilic pneumonia rather than persistent eosinophilia in the lung and that a short course of steroid therapy may effectively control acute eosinophilic pneumonia.
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PMID:Activation of lymphocytes and increased interleukin-5 levels in bronchoalveolar lavage fluid in acute eosinophilic pneumonia. 1083 52

Several studies have been carried out to clarify the relationship between CD30 expression and Th2 lymphocytes, although the results have been controversial. To investigate whether CD30 is a useful marker for Th2 lymphocytes in bronchoalveolar lavage (BAL) in interstitial lung diseases (ILD), we studied six control subjects and 31 patients with ILD (12 with idiopathic pulmonary fibrosis, seven with hypersensitivity pneumonitis, three with chronic eosinophilic pneumonia and nine with sarcoidosis). The levels of interleukin-5 (IL-5) (secreted by Th2 cells), interferon-gamma (IFNgamma) (secreted by Th1 cells) and the expression of CD30 on lymphocytes were determined in BAL fluid. There were no differences in the percentage of CD30+ lymphocytes between controls and patients with ILD (0.8+0.4% vs. 2+/-0.4%). In order to determine the relationship between Th2 cells and CD30 expression, we divided the patients into two groups according to BAL IL-5 levels. Group I consisted of eight patients (three chronic eosinophilic pneumonia, three hypersensitivity pneumonitis, two idiopathic pulmonary fibrosis) with high IL-5 levels (298+/-138 pg ml(-1)). Group II consisted of the remaining 23 ILD patients with normal IL-5 levels (0.9+/-0.6 pg ml(-1)). The percentage of eosinophils in BAL fluid was significantly higher in group I compared with group 11 (34+/-16% vs. 3+/-1%, P < 0.05). A correlation between CD30+ lymphocytes and IL-5 in group 1 was not shown. There were no differences in the number of CD30+ I we found a significant correlation between IL-5 levels and the percentage of eosinophils (r = 0.95, P < 0.0001). Our results suggest that CD30 does not appear to be a useful marker for Th2 lymphocytes in BAL from patients with ILD.
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PMID:Evaluation of CD30 as a marker for th2 lymphocytes in bronchoalveolar lavage in interstitial lung diseases. 1084 32

A 76-year-old woman who had complained of cough and productive sputum since mid-January, 1999, was admitted to our hospital with fever and dyspnea on February 4, 1999. She had been treated with levofloxacin at an outpatient clinic. On admission, she had orthopnea, and auscultation revealed coarse crackles and wheeze in the bilateral lung fields. Chest x-ray and CT films showed non-segmental infiltration in bilateral lung fields. Laboratory data revealed eosinophilia in peripheral blood (= 24%) and sputum (= 10%), airflow limitation, hypoxemia (PaO2: 46 Torr), and increased airway responsiveness to methacholine (Dmin: 0.127 units). A bronchoalveolar lavage (BAL) fluid showed increased total cells and a 55% increase in eosinophils, and CD4/CD8 ratio was decreased to 0.8. In addition, IL-5 was increased in BAL fluid. Transbronchial lung biopsy specimens revealed infiltrations of eosinophils in the alveolar and interstitial compartments. Histological features of the bronchial biopsy specimens included increased eosinophils in the submucosa and goblet cell metaplasia. The woman was diagnosed with eosinophilic pneumonia complicated by bronchial asthma. She was given theophylline, pranlukast hydrate, and an inhaled beta 2 receptor agonist (procaterol hydrochloride), and pre-admission drugs including Levofloxacin were discontinued. Her symptoms were improved, peak expiratory flow rate and PaO2 increased, airway responsiveness to methacholine decreased (Dmin: 0.615 units), and radiographic abnormalities disappeared without steroid therapy. A leukocyte migration test for levofloxacin was weakly positive. An environmental provocation test in the patient's home gave negative results. A challenge test for levofloxacin was not performed due to a lack of informed consent. Based on these findings, we diagnosed this case as levofloxacin-induced lung injury manifesting as eosinophilic pneumonia complicated by bronchial asthma. Levofloxacin should be added to the list of agents that can produce eosinophilic pneumonia.
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PMID:[Levofloxacin-induced eosinophilic pneumonia complicated by bronchial asthma]. 1092 Dec 86

The purpose of this study was to evaluate the role of several eosinophil growth factors including interleukin (IL)-5, interleukin (IL)-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) in the pathogenesis of interstitial lung disease with eosinophilia. IL-5, IL-3 and GM-CSF in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA) in patients with eosinophilic pneumonia (EP), bronchiolitis obliterans organizing pneumonia (BOOP), idiopathic pulmonary fibrosis (IPF), sarcoidosis and healthy volunteers. IL-5 in BALF was high only in patients with EP. IL-3 in BALF was undetectable in the majority of patients with these diseases. GM-CSF in BALF was detectable in 30-67% of each group of patients. In patients with BOOP and IPF, the number of eosinophils in BALF was higher in patients with detectable GM-CSF than in patients in whom GM-CSF was below the detection limit. Eosinophil cationic protein (ECP) was detected in all patients with EP and some with BOOP and IPF. There was a significant correlation between ECP levels and percentage or number of eosinophils in BALF. The results suggest the possibility that interleukin 5 in eosinophilic pneumonia, and granulocyte-macrophage colony-stimulating factor in bronchiolitis obliterans organizing pneumonia and idiopathic pulmonary fibrosis may play important roles in eosinophil recruitment in the lung. Activation of eosinophils in the lung is likely to be induced by both interleukin 5 and granulocyte-macrophage colony-stimulating factor.
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PMID:Interleukin 5 and granulocyte-macrophage colony-stimulating factor levels in bronchoalveolar lavage fluid in interstitial lung disease. 1115 99

To clarify the pathogenesis of chronic eosinophilic pneumonia (CEP), the apoptosis of eosinophils from bronchoalveolar lavage (BAL-Eos) was compared with that of eosinophils from peripheral blood (PB-Eos) in six cases of CEP. The survival rate of eosinophils and the percentage of apoptotic cells of both types of eosinophils were examined, and the effects of interleukin 5 (IL-5) were evaluated. The role of Fas expression in apoptosis of these eosinophils was also studied. The survival rate of BAL-Eos on the third day of culture was significantly higher than that of PB-Eos (p < 0.01). This was associated with a lower proportion of apoptotic cells in BAL-Eos than in PB-Eos; the percentages of apoptotic cells in PB-Eos and BAL-Eos after 24 h of incubation were 21.7 +/- 3.4% and 10.6 +/- 1.7% respectively. IL-5 suppressed apoptosis and increased the survival rate of both PB-Eos and BAL-Eos. It was found that the apoptotic character of BAL-Eos differed from that of PB-Eos in at least three ways. Firstly, the positive rate of Fas expression on PB-Eos was increased after 24 h of incubation, whereas that on BAL-Eos did not change. Secondly, the expression of Fas on PB-Eos was suppressed by IL-5 (18.5 +/- 4.2% - 8.3 +/- 3.2%, p < 0.05), whereas IL-5 failed to suppress Fas expression on BAL-Eos (3.3 +/- 1.6% - 3.6 +/- 1.0%). Lastly, binding of antibody to Fas antigen induced apoptosis of PB-Eos, but not of BAL-Eos. These data suggested that Fas seemed to be involved in the apoptosis of PB-Eos, whereas BAL-Eos were Fas-resistant in chronic eosinophilic pneumonia. In conclusion, apoptosis of eosinophils might be suppressed by proinflammatory cytokines such as IL-5 leading to their accumulation in the lung. Chronic stimulation of eosinophils in the alveolar space with IL-5 may play a crucial role chronic eosinophilic disorders.
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PMID:Apoptotic response of eosinophils in chronic eosinophilic pneumonia. 1133 18

Drugs induce a variety of pulmonary diseases including pulmonary infiltration with eosinophilia (PIE) syndrome. We report a case of PIE syndrome which was observed after neck dissection. An 83-year-old male patient attended our clinic complaining of upper neck swelling and was diagnosed as advanced lymph node metastasis related to previously resected oral carcinoma and underwent neck dissection. Despite administration of antibiotics (piperacillin sodium, PIPC; and tosufloxacin tosilate, TFLX), fever and an elevation of the c-reactive protein (CRP) level with neutrophilia appeared, and an infiltration shadow was observed in the right lower pulmonary field. With the suspicion of pneumonia, the antibiotics were exchanged for panipenem/betamipron. However, the pulmonary infiltration spread widely, CRP increased to 12.9 mg/dl and severe eosinophilia (23%) was observed a few days after changing the antibiotics. PIE syndrome was suspected, and the patient underwent steroid mini-pulse therapy consisting of methylprednisolone sodium succinate (500 mg) and prednisolone (60 mg). After steroid therapy, the pulmonary condition largely improved. However, about 2 weeks after the start of steroid administration, a fever and a further elevation of CRP were observed with an increase of beta-D-glucan in serum. Roentgenography revealed diffuse infiltration shadows throughout the lungs, and the patient died about 3 weeks after the onset from respiratory distress. In vitro, blastogenesis of patient's peripheral blood lymphocytes was strongly enhanced by PIPC and TFLX, and they generated a large amount of interleukin-5 in the presence of PIPC or TFLX. The clinical course and laboratory examination results revealed that PIE syndrome may have been induced by PIPC and TFLX and that PIE syndrome should be suspected in treatment of carcinomas when dyspnea and pulmonary infiltration are complicated with eosinophilia.
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PMID:Pulmonary infiltration with eosinophilia (PIE) syndrome induced by antibiotics, PIPC and TFLX during cancer treatment. 1137 37

A 17-year-old girl was admitted to our hospital because of acute febrile illness, progressive dyspnea and severe hypoxemia. Chest radiography and HRCT showed bilateral diffuse ground-glass opacities, consolidation, Kerley lines and pleural effusion. Analysis of bronchoalveolar lavage fluid showed 41.9% eosinophils, and a transbronchial lung biopsy revealed infiltration of eosinophils into the alveolar septa and mild alveolar septal edema. The patient's condition was improved immediately by corticosteroid therapy. She had begun smoking and taking health food (chitosan) 3 months before the admission. A smoking challenge test was positive and a drug-induced lymphocyte stimulation test for chitosan was positive. These findings suggested acute eosinophilic pneumonia caused by smoking and health food. The concentration of interleukin-5 (IL-5) in the serum and BALF/granulocyte colony-stimulating factor (G-CSF) in the serum on admission were very high, but decreased after the improvement. Therefore, it is likely that IL-5 and G-CSF are important in the onset of acute eosinophilic pneumonia.
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PMID:[Acute eosinophilic pneumonia with positive response to smoking challenge test, suggesting the involvement of health food]. 1151 Jan

While much progress has been achieved in controlling infectious diseases, there is a startling increase in the prevalence of allergic disorders in developed countries. Previous studies using experimental murine models of asthma have demonstrated that mycobacterial infections are capable of suppressing asthma-like reactions induced by ovalbumin (OVA). Using a different intracellular bacterium, Chlamydia trachomatis mouse pneumonitis (MoPn), we examined the effect of infection on the development of allergic responses to a common natural airborne allergen, ragweed (RW). The data showed that airway eosinophilia induced by ragweed sensitization/challenge was significantly reduced in MoPn-infected mice. MoPn-infected mice also exhibited significantly lower levels of allergen-driven Th2 cytokine production, namely IL-4, IL-5, IL-10, and IL-13, following ragweed exposure in comparison with those treated with ragweed only. Additionally, the production of eotaxin, a C-C chemokine for eosinophil chemoattraction following RW exposure, was significantly reduced in the lungs of MoPn-infected mice. However, MoPn infection did not reduce the levels of RW-specific IgE and IgG1 production in the sera, nor did it diminish the level of total serum IgE. These data provide evidence that the suppression of the allergic airway inflammation induced by a common environmental allergen is attainable through intracellular bacterial infection.
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PMID:Chlamydia trachomatis infection inhibits airway eosinophilic inflammation induced by ragweed. 1178 Oct 65

Thymus- and activation-regulated chemokine (TARC/CCL17) is a lymphocyte-directed CC chemokine, which plays a role in the recruitment of CC chemokine receptor-4 positive T helper 2 (Th2) cells. In this study, we measured concentrations of TARC and Th2 cell-derived cytokines in bronchoalveolar lavage (BAL) fluid, as well as TARC concentrations in serum from patients with eosinophilic pneumonia and other interstitial lung diseases. TARC was significantly elevated in BAL fluids from patients with eosinophilic pneumonia (median, 240 pg/ml), whereas TARC was undetectable (< 7 pg/ml) in most cases of hypersensitivity pneumonitis, sarcoidosis, and idiopathic pulmonary fibrosis, as well as in healthy control subjects. Also, when present, quantities were less than 20 pg/ml. Elevated concentrations of interleukin (IL)-4, IL-5, and IL-13 were also detected in BAL fluid from patients with eosinophilic pneumonia. Interestingly, TARC concentrations in BAL fluids were closely correlated with the concentrations of IL-5 and IL-13. A serial examination showed that elevated TARC in BAL fluid rapidly fell to below detectable limits preceding decreases in IL-5 concentration and eosinophil percentage. Our results, in concordance with previous studies, demonstrate the potential activity of TARC for recruiting Th2 cells to the lungs and suggest a significant role for TARC in the pathogenesis of eosinophilic pneumonia.
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PMID:Elevated levels of thymus- and activation-regulated chemokine in bronchoalveolar lavage fluid from patients with eosinophilic pneumonia. 1195 56

Interleukin-5 (IL-5) plays an important role in allergic diseases accompanied by eosinophilia. We examined IL-5 messenger RNA (mRNA) expression in peripheral blood mononuclear cells (PBMC) isolated from 13 patients with bronchial asthma, 1 patient with chronic eosinophilic pneumonia, 2 patients with idiopathic eosinophilia, and 5 control subjects. IL-5 mRNA was expressed in PBMC from 2 of 13 patients with asthma, 1 patient with chronic eosinophilic pneumonia, and 1 of 2 patients with idiopathic eosinophilia. IL-5 mRNA expression was not detected in PBMC from control subjects. PBMC from a patient with chronic eosinophilic pneumonia expressed IL-5 mRNA spontaneously. Prednisolone treatment decreased his clinical symptoms and IL-5 mRNA expression. IL-5 mRNA expression preceded revival of the disease. These observations show that IL-5 plays a role in the condition, accompanied by eosinophilia, and IL-5 mRNa examination in PBMC by means of reverse transcription-polymerase chain reaction may be useful to predict the activity of eosinophilia.
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PMID:Interleukin-5 messenger RNA expression in peripheral blood mononuclear cells from patients with bronchial asthma and eosinophilia. 1212 4

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