Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhalation of aerosolized ovalbumin by guinea pigs both during sensitization and upon challenge induces a pulmonary eosinophilia as assessed by cells recovered in bronchoalveolar lavage fluid (BALF). In comparison with BALF eosinophil numbers in naive animals of 0.82 +/- 0.2 x 10(6) cells, those in sensitized animals before challenge and 17 and 72 h after challenge were 1.48 +/- 0.2 x 10(6), 2.60 +/- 0.6 x 10(6), and 4.2 +/- 0.7 x 10(6) cells, respectively. BALF eosinophils from all these groups were notable for their heterogeneity with respect to density, size, and appearance under the electron microscope. In comparison with peritoneal eosinophils, which had a single mean density peak of 1.088 +/- 0.001 g/ml, BALF cells comprised hypodense (less than 1.080 g/ml), normodense (1.080 to 1.096 g/ml), and hyperdense (greater than 1.096 g/ml) eosinophils. The percentage of hypodense eosinophils rose from 25% in naive animals to 63% in sensitized animals (P less than 0.001) and fell after challenge. In contrast, challenge induced the appearance of hyperdense eosinophils, which rose from 6% in sensitized animals to 42% 72 h after challenge (P less than 0.001). Blood eosinophils in naive animals showed a similar profile to those in the lung, but after sensitization and challenge no gross changes in the proportion of either hypodense or hyperdense eosinophils were observed. Flow cytometric analysis of BALF eosinophils indicated that hypodense eosinophils, with a mean diameter of 15.8 microns, were larger than both normodense and hyperdense eosinophils, which had mean diameters of 14.3 and 11.6 microns, respectively. Although the numbers and size of granules were not reduced in hypodense BAL eosinophils, electron microscopy morphology indicated a reduced granular content.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Density profile of bronchoalveolar lavage eosinophils in the guinea pig model of allergen-induced late-phase allergic responses. 154 Mar 98

Patients with HES and pulmonary infiltrates may pose certain diagnostic problems as the infiltrates may be attributed to infection, infarction, congestive heart failure, or HES itself. We report an 87-year-old woman with idiopathic HES presenting with bibasal alveolar infiltrates. Differential cell count in BAL fluid yielded a very high percentage (73 percent) of eosinophils. Other authors previously mentioned the absence of eosinophils in the lavage fluid despite an important peripheral eosinophilia in a patient with the idiopathic HES but without HES-related pulmonary involvement. Thus, BAL fluid eosinophilia may suggest HES-related pulmonary involvement. Therefore, BAL might be an important diagnostic tool in the management of pulmonary infiltrates in idiopathic HES.
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PMID:Idiopathic hypereosinophilic syndrome-related pulmonary involvement diagnosed by bronchoalveolar lavage. 155 50

Asthmatics can have a blood eosinophilia which in some studies correlates with the severity of the disease. However, an increased number and percentage of activated eosinophils can be present in the blood without asthma. The eosinophils that contribute to asthma will be those in the lung. In the BAL fluids collected from asthmatics there is usually no change in total cell number, but there are changes in the differential cell count. A consistent finding is an increase in percentage of mast cells and eosinophils with a tendency for an increase in lymphocytes and epithelial cells and a decrease in percentage of macrophages. As with the blood eosinophilia, an increase in number of eosinophils can be present in BAL fluids without asthma. The site of localization and activation of the eosinophils in the lung may be critical. In bronchial biopsies, taken from asthmatics, increased number of mast cells, eosinophils and lymphocytes have been demonstrated in the bronchial mucosa together with shedding of columnar epithelial cells. However these changes have not been found, or have not reached significance, in all studies. An increase in number of activated eosinophils and T-lymphocytes has been demonstrated but an increase in number of degranulating mast cells has been disputed. A consistent finding has been thickening below the basement membrane. Attempts to correlate the changes in the BAL or lung biopsies with the severity of asthma, lung airways function or bronchial responsiveness have given inconsistent results. Treatment of asthmatics with inhaled steroids can reduce the cellular infiltration in the bronchial biopsies to normal levels but this produces a trivial reduction in bronchial responsiveness. It is possible that infiltration of inflammatory cells into the bronchial mucosa is intermittent, at least in mild asthma, but this produces changes leading to a long lasting bronchial hyperresponsiveness.
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PMID:Asthma, inflammation, eosinophils and bronchial hyperresponsiveness. 157 12

Previous studies from our laboratory have demonstrated a temporal relationship between eosinophil influx into the airways and the onset of airway hyperresponsiveness to inhaled methacholine. The purpose of the present study was to extend this observation by evaluating changes in airway cellular composition and measuring the levels of granulocyte-derived mediators recovered in BAL fluid during the onset and recovery from antigen-induced airway hyperresponsiveness. Airway cellular composition, airway responsiveness to inhaled methacholine and the levels of BAL fluid EPO and MPO were monitored over a 32 day study in eight adult male Ascaris suum sensitive cynomolgus monkeys. Repeated Ascaris suum inhalation (nine challenges during days 0-21) resulted in a selective, sustained airway eosinophilia that was temporally related with the onset and maintenance of airway hyperresponsiveness (r = 0.67, P less than 0.001). The level of BAL eosinophil-derived EPO was increased and remained elevated concurrent with the increase in airway eosinophils and airway responsiveness. During the recovery phase (days 22-32) the actual number of eosinophils remained elevated, while BAL EPO levels were significantly decreased. The recovery phase was also associated with a transient increase in the number of BAL neutrophils and MPO concentration. We conclude that the number and state of activation of airway eosinophils directly correlate with the onset and maintenance of airway hyperresponsiveness. Recovery from airway hyperresponsiveness is associated with a decrease in eosinophil activation and a transient increase in the number of activated neutrophils.
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PMID:The onset and recovery from airway hyperresponsiveness: relationship with inflammatory cell infiltrates and release of cytotoxic granule proteins. 157 22

Three radiologically and bacteriologically confirmed pulmonary tuberculosis patients had eosinophilic pneumonia, as demonstrated by BAL. In two patients, pulmonary eosinophilia was present only at the site of the lesion and the third had eosinophilia in both peripheral blood and lung. There was complete elimination of the eosinophilic inflammatory process in two patients who had successfully completed antituberculosis treatment.
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PMID:Pulmonary eosinophilia in pulmonary tuberculosis. 160 Jul 96

Inhalation of aerosols of ovalbumin in sensitized guinea pigs produced a marked, bronchoalveolar eosinophilia 24 hr after challenge. The lung eosinophilia was not prevented by the cyclooxygenase inhibitors, indomethacin or PAF antagonists (WEB-2086 and L-652731) but was inhibited by methylprednisolone, the 5-LO inhibitor, U-66858 and a series of structural analogs of LTB4, U-75302, U-77692, U-75485 and U-78489. The effectiveness of LTB4 antagonists but not PAF antagonists in vivo was consistent with in vitro studies in which LTB4 was shown to be far more chemotactic than PAF for guinea pig eosinophils. LTB4 elicited maximal directional migration of guinea pig eosinophils at concentrations from 10(-7) M to 10(-9) M while PAF showed no effect over the same concentration range. The structural analogs of LTB4 were shown to inhibit LTB4 induced chemotaxis of guinea pig eosinophils and produced a dose-related inhibition of binding of LTB4 to guinea pig eosinophil membranes. To add further proof to the hypothesis that LTB4 contributed to the antigen-induced lung eosinophilia we attempted to measure LTB4 release into BAL fluid immediately after and at various time points up to 24 hr after antigen inhalation. However, using a sensitive radioimmunoassay (detection limit 10 pg/ml) very low levels of LTB4 (24.9-67.9 pg/ml) or its metabolite, 20-OH LTB4 (24.9-98.2 pg/ml) were detected in BAL fluid and these levels did not increase significantly following antigen provocation. Inhalation of LTB4 aerosols in unsensitized Brown-Norway rats or inhalation of aerosols of ovalbumin in sensitized Brown-Norway rats also produced a marked "late-phase" eosinophil-rich influx of inflammatory cells into the lungs. The lung eosinophilia in the rat was prevented by two structurally unrelated leukotriene B4 (LTB4) antagonists, U-75302 and Ly255283. These data implicate LTB4 as a mediator of allergen-induced bronchopulmonary eosinophilia. Leukotriene B4 antagonists may provide leads for the development of compounds which inhibit the chronic airway inflammation associated with asthma in man.
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PMID:Contribution of leukotriene B4 to airway inflammation and the effect of antagonists. 165 82

Exposure of normal guinea pigs to an aerosol of PAF induced an increase in airway responsiveness to i.v. histamine, 24 h and 48 h post challenge compared to animals that received BSA alone. There was no significant alteration in airway responsiveness 1 h, 4 h or 72 h after PAF challenge. Exposure of actively sensitised guinea pigs to an aerosol of ovalbumin induced airway hyperresponsiveness to i.v. histamine, 24 h post challenge. PAF induced a selective increase in the percentage of eosinophils in bronchoalveolar lavage fluid 24 h after challenge, that persisted for at least 72 h post challenge. No significant increase in eosinophils was noted 1-4 h after PAF exposure. Antigen challenge of actively sensitised guinea pigs induced a significant increase in the percentage of eosinophils recovered in BAL fluid 24 h post challenge. Pretreatment of both normal and sensitised guinea pigs with the selective PAF antagonist WEB 2170 significantly inhibited both airway hyperresponsiveness and airway eosinophilia 24 h post challenge with aerosol PAF or allergen. These results further support the suggestion that PAF may play a central role in allergen induced eosinophil infiltration and airway hyperresponsiveness in the guinea pig.
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PMID:The effect of the selective PAF antagonist WEB 2170 on PAF and antigen induced airway hyperresponsiveness and eosinophil infiltration. 189 85

Airway hyperresponsiveness is an important and characteristic feature of asthma. In monkeys, we have reported that antigen (Ag) inhalation induces a prolonged airway eosinophilia, that chronic airway eosinophilia is associated with marked airway hyperresponsiveness, and that chronic Ag inhalations induce airway eosinophilia and hyperresponsiveness. In this study we have determined the effects of acute Ag inhalation(s) on airway responsiveness to obtain a protocol for the study of the mechanisms involved. Anesthetized and intubated adult male cynomolgus monkeys with a naturally occurring sensitivity to Ascaris suum extract were studied. Airway responsiveness (provocative concentration of nebulized and inhaled methacholine that induced a 100% increase in respiratory system resistance [Rrs] [PC100]; twofold decrease regarded as significant) and airway cell composition (bronchoalveolar lavage [BAL]) were determined 1 day before and 20 hours after a single inhalation of Ascaris extract, or 3 days before and 3 days after three alternate-day inhalations of Ascaris extract. The single inhalation of Ag (N = 7) caused an acute increase in Rrs (307% +/- 62%), an increase in BAL leukocytes, and a decrease in PC100 in three animals that was moderate (more than eightfold) in two animals. The mean +/- SE change in log PC100 was only -0.25 +/- 0.24. The multiple inhalations of Ag in the same animals caused acute increases in Rrs (178% +/- 48%, 380% +/- 83%, and 331% +/- 63%, respectively), an increase in BAL granulocytes, and a decrease in PC100 in six of seven animals (mean +/- SE change in log PC100 was -1.36 +/- 0.34) that was moderate in two and severe (more than 80-fold) in three animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of single and multiple inhalations of antigen on airway responsiveness in monkeys. 201 78

Fifteen asthmatic patients were prospectively selected. If they had more than 450 eosinophils in peripheral blood on admission to hospital treatment and if before BAL had been performed they were not treated by corticosteroids. No associated disease was found which could cause the increased number of eosinophils in peripheral blood except bronchial asthma. BAL was performed when the subjects tested had no dyspnea, usually 1-3 days after the hospital admission. In contrast to blood eosinophilia, increase of eosinophils number in BAL was found to correlate to impairment of clinically measured parameters such as: ventilation level of blood gases and duration of hospitalisation. On the contrary there was no correlation between the level of blood eosinophilia and gas disturbance and duration of hospitalisation. Eosinophilic proteins (MBP, ECP, EPX, EPO) are not the only that harmfully effect the lung cells in the asthmatic attack but the fact that their level in lavage fluid correlates to eosinophilia degree in BAL is evident so the correlation between the number of eosinophils in BAL and impairment of clinically measured parameters is clear.
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PMID:[Evidence of the harmful effects of eosinophils in bronchial asthma]. 221 19

A 54-year-old female with bronchial asthma and PIE syndrome induced by disodium cromoglycate (DSCG) was reported. She was referred to our hospital for further examination of the abnormal chest shadows and eosinophilia. She had been treated with DSCG, Cefaclor. Bromhexine and bronchodilator for bronchial asthma and bronchitis. Withdrawal of the drugs except for the bronchodilators alleviated her symptoms. Therefore, drug induced lymphocytes stimulation tests (DLST) were performed for those three drugs. Only DLST for DSCG showed a positive result. She had been asthmatic for ten years and treated by the drug for 18 months prior to admission. The skin test for the drug was negative and a precipitating antibody for the drug could not be found. To obtain a definite diagnosis, bronchial challenge by DSCG was performed, after her symptoms were under control. Severe asthmatic responses were provoked in 6 and 24 hours after the inhalation of DSCG. Bronchoalveolar lavage, performed 8 days after the provocation, revealed increased eosinophils and lymphocytes in BAL fluid. Although several cases of PIE syndrome induced by DSCG have been reported, this seems to be the first report of late and delayed type bronchial response and pulmonary infiltration with eosinophilia provoked by DSCG. The bronchial response to the drug was a late and delayed type reaction and sustained for a long period. This might indicate that PIE syndrome induced by the drug may be caused by a same mechanism as the provoked asthmatic response.
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PMID:[A case of bronchial asthma and PIE Syndrome induced by disodium cromoglycate]. 250 49


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