Superoxide dismutase activity in the broncho-alveolar lavage fluid in late asthmatic response model in guinea pigs]

In order to investigate the mechanism of the late asthmatic responses (LAR), LAR model in guinea pigs was made by inhalation of a large quantity of egg albumin antigen. Serial changes of inflammatory cells and superoxide dismutase activities in broncho-alveolar lavage fluids obtained from these animals were observed. In this model, increase in inflammatory cells, such as neutrophils, was observed in the broncho-alveolar lavage fluid during the late asthmatic responses of the attack and superoxide dismutase activity increased in the broncho-alveolar lavage fluid in parallel with the increase in inflammatory cells. These results suggest that change in superoxide dismutase activity in the broncho-alveolar lavage fluid may be involved in the onset of the late asthmatic responses.     

Cyclosporine A inhibits allergen-induced late asthmatic response and increase of airway hyperresponsiveness in guinea pigs]

Considerable interest has recently focused on the role of T-cell function in the pathogenesis of asthma. We have previously demonstrated that repeated inhaled antigen (ovalbumin; OA) exposure resulted in an appearance of late phase airway obstruction (LAR) in more than 50% and significant increase of airway hyperresponsiveness (AH) in guinea pig experimental models. We have studied the effect of cyclosporine A (CsA), a potent helper T-cell suppressant, on these models in vivo. Respiratory resistance (Rrs) of sensitized guinea pigs by repeated OA inhalation was measured by the oscillation method and AH estimated as an inhaled concentration of histamine, causing a 200% increase in the baseline Rrs (PC200 Hist). The magnitude of immediate OA (10 mg/ml/min) inhalation-induced bronchoconstriction was not significantly different in CsA-treated (25 mg/kg/day, 7-day oral administration) and non-treated groups. However, the development of LAR was markedly inhibited in CsA treatment groups (n = 5). Antigen-induced increase of AH at 24 hr and 5 days was also significantly inhibited by CsA pretreatment. We conclude that CsA is capable of inhibiting the development of LAR and increase of AH, and thus the regulation of T-cell function may contribute to the treatment of asthma.     

Bronchoalveolar eosinophilia during allergen-induced late asthmatic reactions

In order to obtain information about the nature of the local inflammatory process during late asthmatic reactions after house dust mite inhalation, bronchoalveolar lavage (BAL) was performed in 19 asthmatic patients and in 5 control subjects. In 16 of the patients and in all of the control subjects, BAL was performed 6 to 7 h after allergen inhalation. Six of the patients showed early and late asthmatic reactions (LAR), 5 showed early reactions, and 5 showed no reactions. Bronchoalveolar lavage was also performed shortly after the early reaction in 5 patients with documented combined early and late reactions. In the BAL fluid of the patients with LAR, a significant eosinophilia (0.01 less than p less than 0.05) was found compared with that in all other patient groups and with that in the control subjects. This bronchoalveolar eosinophilia was accompanied by elevated eosinophil cationic protein/albumin ratio in the BAL fluid (0.01 less than p less than 0.05). These observations suggest that eosinophils and their mediators might be involved in the development of LAR after allergen inhalation.     

Bronchoalveolar lavage does not alter airway responsiveness in asthmatic subjects

Bronchoalveolar lavage (BAL) during fiberoptic bronchoscopy is being used increasingly for the investigation of asthma. Airway responsiveness to methacholine is a sensitive indicator of the presence and severity of asthma. Therefore, we studied the effect of BAL on methacholine airway responsiveness in stable asthmatics. Geometric mean methacholine PC20 was 1.34 mg/ml before and 1.80 mg/ml after BAL (p = 0.26) in asthmatics. Immediate symptoms of airway narrowing after BAL occurred only in the 3 asthmatics with moderate to severe hyperresponsiveness. These symptoms were rapidly relieved by inhaled bronchodilator. There was no relationship between the occurrence of symptoms and the amount of topical lidocaine used for local anaesthesia or the volume of lavage fluid returned. The absence of an effect of BAL on airway responsiveness supports the safety of this procedure in the controlled asthmatic patient with near normal FEV1, irrespective of the level of baseline airway responsiveness.     

Bronchoalveolar neutrophilia during late asthmatic reactions induced by toluene diisocyanate

The mechanism by which late asthmatic reactions are induced by toluene diisocyanate (TDI), a low molecular weight chemical that causes occupational asthma in exposed subjects, is unknown. We investigated whether early and late asthmatic reactions induced by TDI are associated with changes in airway responsiveness to methacholine and airway inflammation as determined by bronchoalveolar lavage. We measured FEV1 before and at regular intervals after exposure to TDI, and performed dose-response curves to methacholine and bronchoalveolar lavage at 8 h after TDI in a group of 6 subjects with late asthmatic reactions and in 6 subjects with only early asthmatic reactions. The same procedure was followed 2 h after TDI in a group of 6 subjects with previously documented late asthmatic reactions and in a group of 6 subjects without any previously documented asthmatic reaction after TDI. In subjects with late asthmatic reactions, neutrophils were increased at both 2 and 8 h, and eosinophils and airway responsiveness were increased only at 8 h. By contrast, neutrophils, eosinophils and airway responsiveness were not increased at 8 h after TDI in subjects with an early asthmatic reaction or at 2 h after TDI in normal control subjects. These results suggest that late asthmatic reactions to TDI, and the associated increase in airway responsiveness, may be caused by airway inflammation.     

Bronchoalveolar lavage in sarcoidosis

There is no single cell type present in bronchoalveolar lavage (BAL) fluid that appears to be predictive for sarcoidosis. However, BAL fluid analysis can be very helpful in the differential diagnosis. A grouping of features, an elevated total cell count, predominantly lymphocytes, together with a nearly normal percentage of eosinophils and polymorphonuclear neutrophils and the absence of plasma cells, distinguish the most likely diagnosis of sarcoidosis from the most common interstitial lung diseases, extrinsic allergic alveolitis (EAA), nonspecific interstitial pneumonia (NSIP), and idiopathic pulmonary fibrosis (IPF). In sarcoidosis the majority of cases have an increased number of lymphocytes and a normal amount of eosinophils and neutrophils. Disease presentation or activity at the time the BAL is performed as well as the smoking status is crucial for interpretation of individual BAL fluid analysis results. In severe cases the number of neutrophils can be increased as well. For an individual case the CD4:CD8 ratio is of less importance because it can be increased, normal, and even decreased. In the follow-up depicting prognosis and response to treatment, BAL fluid analysis has less clinical relevance.     

Bronchoalveolar lavage in silicosis

In this report we describe the chronic effects of inhaled silica, a potent macrophage toxin, on cells which could be lavaged from the lung in man. Eight bronchoalveolar lavages were performed on patients with complicated silicosis, who had last been exposed to silica 1 to 12 years prior to lavage. We compared the results with those from 10 lavaged control subjects. All subjects in both groups were cigarette smokers. No differences were detected in cell number, viability, adherence or ability to phagocytize and killListeria monocytogenes, but significantly increased numbers of type II pneumocytes were present in lavages from the silicotic subjects. This finding probably indicates type II cell hyperplasia and provides indirect evidence of the continuing presence of biologically active material within the lung years after cessation of exposure to silica.     

Suplatast tosilate inhibits late response and airway inflammation in sensitized guinea pigs.

The effect of suplatast tosilate, which has been proven to inhibit T-cell synthesis of IL-4 and IL-5, on the response to antigen inhalation challenge was investigated in sensitized guinea pigs. The animals were given an oral dose of 30 or 100 mg/kg of suplatast or vehicle (distilled water) daily for 1 wk before antigen challenge. Measurement of pulmonary resistance for 6 h was followed by bronchoalveolar lavage and lung fixation. After antigen challenge, all guinea pigs in the vehicle group displayed dual-phase airway obstruction and accumulation of eosinophils and lymphocytes in the airways. After 1 wk of treatment with the high dose of suplatast, the late asthmatic response and the recruitment of eosinophils and lymphocytes into the airways were significantly inhibited, but the early asthmatic response was not affected. In situ hybridization revealed that challenge-induced increases in IL-5 mRNA-positive cells in lung tissue were significantly inhibited after treatment. Thus, suplatast inhibited airway obstruction in the late phase by specifically inhibiting the inflammatory process after mast cell degranulation.     

Bronchoalveolar lavage in malignancy

Bronchoalveolar lavage is a useful diagnostic tool in diffuse or disseminated lung malignancies that do not involve the bronchial structures visible by endoscopy. The neoplastic histotype and the intraparenchymal neoplastic growth pattern are good predictors for diagnostic yield; adenocarcinoma, and tumors with lymphangitic or lepidic growth patterns are more easily diagnosed by bronchoalveolar lavage; in these cases the diagnostic yield reported is higher than 80%. In hematologic malignancies the diagnostic yield is quite good in secondary diffuse indolent B cell lymphomas and in primary B cell lymphomas of mucosa-associated lymphoid tissue (MALT) type but low in Hodgkin disease. Morphological analysis may be implemented by immunocytochemical or molecular tests to identify the cell lineage and the presence of monoclonality. Disorders in which bronchioloalveolar cell hyperplasia/dysplasia is a significant morphological component may have cytological features in bronchoalveolar lavage fluid that mimic lung neoplasms: acute respiratory distress syndrome (ARDS), acute interstitial pneumonitis (AIP), and acute exacerbation of idiopathic pulmonary fibrosis are the most important clinical entities in this group.     

Bronchoalveolar lavage in silicosis

In this report we describe the chronic effects of inhaled silica, a potent macrophage toxin, on cells which could be lavaged from the lung in man. Eight bronchoalveolar lavages were performed on patients with complicated silicosis, who had last been exposed to silica 1 to 12 years prior to lavage. We compared the results with those from 10 lavaged control subjects. All subjects in both groups were cigarette smokers.No differences were detected in cell number, viability, adherence or ability to phagocytize and killListeria monocytogenes, but significantly increased numbers of type II pneumocytes were present in lavages from the silicotic subjects. This finding probably indicates type II cell hyperplasia and provides indirect evidence of the continuing presence of biologically active material within the lung years after cessation of exposure to silica.     

Bronchoalveolar lavage in sarcoidosis

Bronchoalveolar lavage (BAL) was performed in 1,188 patients suffering from sarcoidosis. After technical considerations, the authors analyze the results of BAL from a practical point of view concerning its value for the diagnosis of sarcoidosis and its prognostic value and its value for the selection of therapy, particularly for the decision as to steroid treatment. BAL helps in the diagnosis of sarcoidosis, but is not specific enough to provide this diagnosis on its own. The persistence of high alveolar lymphocytosis within the first year of evolution is strongly correlated with nonrecovery from pulmonary sarcoidosis at 2 years and thus with the evolution towards a chronic phase of the disease. On the other hand, BAL can provide basic information for a better understanding of the disease and permits immunocompetent cells and soluble factors to be recovered from the lung, which is useful for immunological studies.     

Bronchoalveolar lavage in asbestosis

The interstitial lung disease associated with asbestosis is unique in that the etiological agent and its effects on the pulmonary parenchyma can be studied on a serial basis using bronchoalveolar lavage. In this way both disease activity and structural derangements can be assessed and used in the treatment of the affected individual. In this review, attention has been drawn to the cascade of inflammatory changes induced by asbestos fibers. The activated inflammatory cells are responsible for the alveolitis characteristic of this condition. Like the other forms of diffuse interstitial lung disease, it is the alveolitis that precedes and predicts eventual fibrosis.     

Bronchoalveolar lavage fluid from asthmatic subjects is mitogenic for human airway smooth muscle

Airway smooth muscle proliferation may contribute to the airway wall remodeling seen in asthma. In this study we tested for the presence of airway smooth muscle mitogenic activity in bronchoalveolar lavage (BAL) fluid obtained from 12 atopic asthmatics before and serially after segmental allergen challenge, and from four normal subjects who did not undergo allergen challenge. Mitogenic effect was assessed by coincubating BAL fluid with human airway smooth muscle cells, and measuring its effect on (3)[H]thymidine incorporation and cell number. Induction of ERK phosphorylation and cyclin D(1) protein abundance were also assessed. Compared with serum-free medium alone, BAL fluid obtained from normal subjects increased thymidine incorporation, cell number, ERK phosphorylation, and cyclin D(1) abundance. BAL fluid from asthmatic subjects prior to allergen challenge induced even greater increases in all measures, except for cell number, which was similar to that observed with normal subjects' BAL fluid. Incubation with lavage fluid obtained 48 h after segmental allergen challenge in atopic asthmatics caused yet further increases in thymidine incorporation, cell number, and cyclin D(1) protein abundance. Molecular sieving of prechallenge BAL fluid from three asthmatic subjects demonstrated that mitogenic activity was present exclusively in the > 10 kD fraction. These results provide the first direct demonstration that fluid lining the airways of asthmatics contains excess mitogenic activity for human airway smooth muscle, and that this activity increases further after allergen challenge.     

Bronchoalveolar lavage in gold lung

We report the results of bronchoalveolar lavage in a patient with gold salt-induced interstitial pneumonitis. The presence of elevated numbers of lymphocytes in the lavage specimen supports a hypersensitivity-related pathogenesis of this disease. Such findings may help distinguish pulmonary complications of gold therapy from interstitial disease due to rheumatoid arthritis.     

Bronchoalveolar lavage in asthma research

Abstract A great deal of information about the pathophysiology of asthma and its treatment have been obtained through the use of bronchoalveolar lavage (BAL), especially in combination with airway biopsies. The introduction of highly sophisticated methods for examining BAL aspirate, including fluorocein activated cell scanning (FACS) analysis and molecular biology techniques has emphasized the potential power of this method of airway investigation. For those contemplating the use of BAL in asthma research programmes, we hope that this review will provide a useful insight into the current state of knowledge about the technique and its application, and that it will provide a solid platform for study design.