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)

To evaluate whether concentrations of cytokines supposed to be involved in eosinophil recruitment and activation were elevated in cystic fibrosis (CF), we assessed interleukin-3 (IL-3), IL-5, IL-8, regulated on activation, normal T-cell expressed and secreted (RANTES); and granulocyte-macrophage colony stimulating factor (GM-CSF) in sputa from 32 patients with CF, eight patients with atopic bronchial asthma, and six patients with bacterial pneumonia. In addition, eosinophil cationic protein (ECP) and eosinophil protein X (EPX) were measured as markers of eosinophil activation. In patients with CF, sputum levels of IL-8 were elevated (p < 0.01) as compared with asthmatic patients. Concentrations of IL-3, ECP, and EPX were not different in the two groups. However, IL-5 (p < 0.0001), RANTES (p < 0.003), and GM-CSF (p < 0.0001) were significantly lower in the CF group than in subjects with asthma. IL-5 was detected only in sputum samples from CF patients with Aspergillus sensitization. In patients with pneumonia, IL-8 levels only were increased. In CF sputum, ECP levels were significantly correlated with the levels of IL-8 (r = 0.626, p < 0.0001) and IL-3 (r = 0.642; p < 0.0001), whereas in asthmatic patients IL-5, IL-8, and RANTES concentrations were significantly related to ECP in sputum. These findings suggest that different cytokine profiles are responsible for eosinophil activation in patients with CF as compared with asthmatic patients. In CF, IL-8 and IL-3 appear to be responsible for increased degranulation of eosinophils.
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PMID:Cytokine concentrations in sputum from patients with cystic fibrosis and their relation to eosinophil activity. 911 85

Acute rejection of the transplanted lung is a clinical problem, since it decreases graft survival and predisposes the patient to chronic rejection and obliterative bronchiolitis (OB). In an earlier study, we had indications that eosinophil cationic protein (ECP) from activated eosinophils and hyaluronan (HYA) from fibroblasts were associated with acute pulmonary rejection. This prospective longitudinal study was designed to investigate whether molecules from activated inflammatory cells in bronchoalveolar lavage (BAL) fluid could serve as clinically useful diagnostic markers for acute rejection. BAL fluid from 138 bronchoscopies performed in 10 single lung, four bilateral lung and five heart-lung transplant recipients were analysed. Nine patients were studied for a period of more than 1 yr (mean 13.4 months) after surgery. Differential cell counts were made from the BAL fluid. ECP, myeloperoxidase (MPO), HYA and interleukin-8 (IL-8) were used as indirect markers for activation and attraction of eosinophils, neutrophils and fibroblasts, respectively. Fifty four episodes of acute rejection were diagnosed. Two patients developed OB. Nine episodes of bacterial infection, 13 episodes of cytomegalovirus (CMV) pneumonitis, three of Pneumocystis carinii infection and one of respiratory syncytial virus (RSV) infection were diagnosed. The mean levels of ECP, MPO, HYA and IL-8 were all higher during rejection episodes, but differences were not statistically significant compared to no rejection, when the confounding factors of time, concomitant infection, and repeated measures in the same individual had been accounted for. We could not confirm that measurements of eosinophil cationic protein, myeloperoxidase, hyaluronan and interleukin-8 in bronchoalveolar lavage fluid can be used as diagnostic markers for acute rejection in the postoperative follow-up of lung transplant recipients.
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PMID:Inflammatory cells and activation markers in BAL during acute rejection and infection in lung transplant recipients: a prospective, longitudinal study. 927 13

The major cause of mortality in the long-term in lung transplant recipients is chronic rejection. This is a fibroproliferative process in the small airways leading to obliterative bronchiolitis and progressive loss of lung function, both constituting the clinical entity bronchiolitis obliterans syndrome (BOS). Granulocyte activation has been implicated as one factor behind BOS. Granulocyte markers in bronchoalveolar lavage (BAL) fluid were prospectively and longitudinally studied in order to identify possible association with BOS. BAL fluid from 266 bronchoscopy procedures performed in twelve single lung, eight bilateral lung and five heart/lung transplant recipients were analysed. The majority (19 of 25) were studied for a period of 2 yrs after surgery. Myeloperoxidase (MPO), eosinophil cationic protein (ECP) and interleukin-8 (IL-8) levels were used as indirect markers of activation and attraction of granulocytes. Five patients developed BOS. Ninety-eight episodes of acute rejection, nine of bacterial infection, 19 of cytomegalovirus pneumonitis, nine of Pneumocystis carinii infection, two of aspergillus infection and two of respiratory syncytial virus infection were diagnosed. BOS patients had significantly higher mean levels of MPO, ECP and IL-8 compared to patients without BOS, irrespective of acute rejection status. Over time, the five patients with BOS had significantly elevated BAL fluid levels of MPO and ECP as well as neutrophil percentages, and in four patients this increase preceded the clinical diagnosis of BOS by several months. Elevated bronchoalveolar lavage fluid neutrophil percentage as well as levels of the granulocyte activation markers myeloperoxidase and eosinophil cationic protein appear to be early signs of development of BOS in lung transplant recipients.
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PMID:Persistent high BAL fluid granulocyte activation marker levels as early indicators of bronchiolitis obliterans after lung transplant. 1059 1

We report a case of Paragonimus westermani infection with a reticulonodular lesion in the right lung, left pleural effusion, and a mobile subcutaneous mass. Analyses of pleural effusion and bronchoalveolar lavage fluid (BALF) showed marked eosinophilia and high levels of eosinophil cationic protein and interleukin (IL)-5. Transbronchial lung biopsy revealed the presence of pneumonia with mild eosinophilic infiltration but remarkable lymphocytic infiltration. In this patient, high IL-5 levels in both BALF and pleural effusion could explain the remarkable eosinophilia.
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PMID:Paragonimiasis westermani with multifocal lesions in lungs and skin. 1083 Jan 72

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

Eosinophils remain among the most enigmatic of cells, as our appreciation of their detrimental activities--e.g., asthma and allergic disease--far outweighs our understanding of their beneficial effects. Among the major secretory effector proteins of eosinophils are the ribonucleases eosinophil-derived neurotoxin (EDN) and eosinophil cationic protein (ECP) in primates and their orthologs, the eosinophil-associated ribonucleases (EARs) in rodents. The rapid diversification observed among these ribonucleases suggested that the ultimate target(s) might be similarly efficient at generating sequence diversity while maintaining an unalterable susceptibility to ribonucleolytic cleavage. This has prompted us to consider a role for these proteins and by extension, for eosinophils, in host defense against single-stranded RNA virus pathogens. We detail our studies of the antiviral activity of eosinophils and eosinophil ribonucleases against respiratory syncytial virus (RSV) in vitro and the related, natural rodent pathogen, pneumonia virus of mice (PVM), in vivo, and consider the possibility that antiviral host defense and the dysregulated responses leading to asthma represent opposing sides of an eosinophil-mediated double-edged sword.
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PMID:Eosinophils, eosinophil ribonucleases, and their role in host defense against respiratory virus pathogens. 1169 87

A relationship between respiratory Chlamydia pneumoniae infection (RCPI) and bronchial asthma is under discussion. Our objective was to study the frequency of RCPI and whether it is associated with markers of asthma in children with recurrent or chronic bronchitis as well as pneumonia. One-hundred and forty-eight children who underwent bronchoscopy were enrolled; 42 children with additional respiratory infections were excluded. Therefore, 106 children were examined, regarding a RCPI, by polymerase chain reaction (PCR) of tracheobronchial aspirate, eosinophilic inflammation of respiratory mucosa (cytology, eosinophilic cationic protein [ECP]), total serum immunoglobulin E (IgE) and specific IgE for six important allergens, as well as lung function tests if possible. There was a RCPI in 55 of 106 children (51.9%); 25.4% of PCR positives (14/55) were weakly positive (double cut-off), which was more prevalent in the 2-5-year age-group and teenagers. Children with RCPI, inclusive of weak positives, showed a milder eosinophilia of nasal mucosa than children without RCPI (5.58% vs. 9.35%, p=0.039). Eosinophilia of > or =13% in nasal- and/or bronchial swab, as a marker for respiratory allergy, was less frequent in patients with RCPI too (7.3% vs. 21.6%, p=0.035). There were no differences in ECP. Total IgE was lower in PCR-positive children (101 vs. 179 IU/ml, p=0.032). Specific IgE with a radioallergosorbent test (RAST) of at least class 3 (as a marker for a relevant allergy), as well as any RAST above zero (to characterize early forms of allergy), were both less frequent in the RCPI group. In contrast, weak positives showed the highest rates of sensitization, surpassing RCPI negatives. In lung-function tests, vital capacity was lower in RCPI patients (87.5% vs. 95.3%, p=0.045); all parameters characterizing obstructive disturbance tended to be higher. Weak positives had both the greatest reduction of vital capacity (75.3%) and the most impaired obstructive parameters. All differences were accentuated in children of 11-18 years of age. Hence, our results indicate that in the children selected, a RCPI is common and not associated with allergic respiratory inflammation. Weak positives, however, differ, having the highest rate of allergic sensitization, reduction of lung volume, and obstructive disturbance. This group might be important in clinically observed asthma after pneumonia caused by C. pneumoniae. In these children, early diagnosis and treatment of a RCPI is recommended.
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PMID:Bronchial Chlamydia pneumoniae infection, markers of allergic inflammation and lung function in children. 1173 72

The mouse eosinophil-associated ribonucleases (mEars) are species specific, divergent orthologs of the human antiviral RNase A ribonucleases, eosinophil-derived neurotoxin (RNase 2) and eosinophil cationic protein (RNase 3). We show here that mEar 2 is also an antiviral ribonuclease, as micromolar concentrations promote a approximately sixfold reduction in the infectivity of pneumonia virus of mice (PVM) for target respiratory epithelial cells in vitro. Although initially identified as a component of eosinophilic leukocytes, mEar 2 mRNA and protein were also detected in lung tissue accompanied by enzymatically active mEar 2 in bronchoalveolar lavage fluid (BALF). At t=3 days post-inoculation with PVM (strain J3666), we observed the characteristic inflammatory response accompanied by diminished expression of total mEar mRNA and protein in lung tissue and a corresponding fivefold drop in ribonuclease activity in BALF. No change in mEar expression was observed in response to infection with PVM strain 15, a replication-competent strain of PVM that does not elicit a cellular inflammatory response. However, mEar expression is not directly dependent on inflammation per se, as diminished expression of mEar mRNA and BAL ribonuclease activity were also observed in PVM-infected, inflammation-deficient, MIP-1alpha -/- mice. We propose that this mechanism may represent a novel virus-mediated evasion strategy, with a mechanism that is linked in some fashion to virus-specific pathogenicity.
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PMID:Diminished expression of an antiviral ribonuclease in response to pneumovirus infection in vivo. 1292 8

BACKGROUND Toxic epidermal necrolysis (TEN) is characterized by widespread erythematous and bullous lesions on the skin. Nowadays, considerable progress has been made in the understanding of its pathogenesis. Immunologically it is similar to graft-versus-host disease. Therefore, we may propose that TEN is a disorder of cell-mediated immunity. CASE REPORT Our patient was a 74-year-old white female who had pneumonia and was positive for hepatitis C virus (HCV), and who had been on levofloxacin therapy. After the first levofloxacin dose, erythematous dusky red macules occurred on her extremities and trunk, and on the following day, confluent purpuric lesions tended to run together over 85% of her body. Her biopsy results indicated TEN. Laboratory testing for serum ECP (eosinophil cationic peptide) and serum immunoglobulin (Ig) levels were performed, and blister fluid was investigated. The patient responded positively to omalizumab treatment and after treatment laboratory tests revealed decreased high sensitive CRP, ECP, IgG1, IgG2, IgG3, IgG4, IgA, and IgM levels. CONCLUSIONS To the best of our knowledge, this is the first case of a patient with HCV who developed cutaneous adverse drug reaction on levofloxacin medication and recovered with omalizumab treatment. This is the first documentation of omalizumab treatment of a TEN patient.
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PMID:Levofloxacin Induced Toxic Epidermal Necrolysis: Successful Therapy with Omalizumab (Anti-IgE) and Pulse Prednisolone. 2763 12

BACKGROUND Eosinophilic pneumonia is recognized both as an eosinophil-associated disease and as bronchial asthma. In eosinophilic pneumonia, the site of eosinophilic infiltration is mainly the alveolus and the peripheral airway; the disability of pulmonary function is restrictive, as opposed to from bronchial asthma, which has a relatively central side bronchus region and obstructive function. Differences in inflammatory region and the activation degree of T-cell and eosinophil parameters were predicted. CASE REPORT To determine the extent of inflammation and the region showing the inflammation in eosinophilic pneumonia, parameters like HLADRCD4/CD4 (%), CD25CD4/CD4 (%), ECP, soluble IL2R, and IL5 were examined in BALF and in peripheral blood during the active phase and remission phase. The percentage of HLADRCD4/CD4, IL-5, and the percentage of CD25CD4/CD4 were extremely high during the acute phase in BALF as compared to that in peripheral blood during the active and the remission phase. To avoid the adverse effects of systemic administration of steroids, we tried 5 different kinds of steroid through inhalation. We used%FVC by spirometry as a parameter to determine the recurrence of the disease. However, the inhaled steroids could not control the remission for long. This is the first report in which frequent recurrence of the disease was seen despite treatments and in which%FVC was used to determine the disease condition. CONCLUSIONS The principle site of inflammation in eosinophilic pneumonia is the peripheral bronchus and the alveolar area. Percent FVC can be a useful parameter for assessment of recurrence of the disease. In the present case, the disease could not be kept under control despite treatment with 5 different steroids through the inhalation route.
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PMID:10-Year Follow-Up of Frequently Relapsed Chronic Eosinophilic Pneumonia Starting at 15 Years Old; Attempts to Treat with Inhaled Corticosteroid (A Case Report). 3118 6


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