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J Y Lacoste

Publications and source records attributed to J Y Lacoste.

14 recordsLinked to original sources
PubMed1992

[Mediators and neuromediators in asthma].

The physiopathological mechanisms underlying the multifactorial syndrome that is asthma are very complex and protean. Most probably, they are genetically determined, but they are largely modulated by the environment and by the inflammation of bronchi in which allergy occupies a special place. Chemical mediators of cellular origin interact with each other and with the cells that live or are recruited in the airways. Among these mediators histamine and arachidonic acid metabolites seem to play a predominant role, but the clinical use of antagonists has not confirmed the data obtained in vitro and in vivo in animals and even man. Cytotoxic mediators (cationic proteins, free oxygen radicals) are though to exert their noxious effect directly on the bronchial epithelium. No single neuromediator of the adrenergic and cholinergic system can explain the dysfunctions observed in asthma. Mediators of the non-adrenergic non-cholinergic system seem to be more interesting owing to their potential interaction with cells and with chemical mediators which contribute to the development of a true neurogenic inflammation.

Asthma↗
PubMed1992

Immunohistochemical characterization of the cellular infiltration in asthmatic bronchi.

Bronchial biopsies obtained from 16 asthmatic patients and six normal subjects were analyzed by immunohistochemistry. In the asthmatic patients, the total numbers of macrophages infiltrating the airway mucosa were increased. Many of the macrophages had the phenotypic characteristics of blood monocytes. HLA Class II antigen was expressed on infiltrating cells and airway epithelial cells. In biopsies from the asthmatics there was a significant increase in activated eosinophils, but not in neutrophils. There was also a significant increase in the numbers of T-lymphocytes in the asthmatics, but very few B-lymphocytes were detected. These results suggest that lung macrophages may have a central role to play in the mechanisms of the chronic immune-mediated inflammatory response seen in the airway mucosa of asthmatic patients.

Adult↗
PubMed1992

Safety of bronchoalveolar lavage and bronchial biopsies in patients with asthma of variable severity.

The safety of fiberoptic bronchoscopy, bronchoalveolar lavage (BAL), and bronchial biopsies has been questioned in asthma, and current recommendations indicate that bronchoscopies should only be performed in mild to moderate asthma. Moreover, in most studies patients receive premedication with nebulized bronchodilators that may enhance the safety of the procedures. The purpose of this study was to determine (1) whether the overall safety of fiberoptic bronchoscopy, BAL, and bronchial biopsies in mild to moderate asthma could be extended to patients with more severe asthma and (2) whether these procedures are safe without premedication with nebulized bronchodilators. A group of 50 patients with asthma of variable severity (FEV1 ranging from 37 to 107% of predicted values) and 25 healthy volunteers were studied. Bronchoscopy, BAL (250 ml), and four bronchial biopsies were performed in a standardized manner, without premedication with a nebulized bronchodilator, by the same investigator. Safety was assessed by clinical follow-up, continuous recording of arterial oxygen saturation during the procedure with a digital oximeter, and measuring FEV1, FEF25-75, and FVC just before and 5 min after bronchoscopy. Arterial oxygen saturation decreased in asthmatic patients from 97% (range 91 to 99%) (T1) to 92% (range 79 to 98%) (T8) (ANOVA, Fisher's PLSD) and in control subjects from 97% (range 94 to 99%) (T1) to 93% (range 88 to 98%) (T8) (ANOVA, Fisher's PLSD). The fall in arterial oxygen saturation was not significantly different between asthmatic and normal subjects, and there was no correlation between arterial oxygen desaturation and the severity of asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Comparison between bronchial and alveolar samples of bronchoalveolar lavage fluid in asthma.

BACKGROUND: Cell content of BALF may vary according to the segment of the lung washed. It was proposed to separate BALF into several aliquots, the first sample being more related to bronchi. The present study compared bronchial and alveolar samples by fractionating aliquots of BALF in normal and asthmatic subjects. METHODS: One hundred asthmatic subjects (mean +/- SEM: 37 +/- 1.5 yr in age) were compared with 31 normal subjects (mean +/- SEM: 32 +/- 2.2 yr in age). None of the subjects was a smoker and none was taking drugs that might interfere with the results. The severity of asthma was defined by the clinical score of Aas examining the chronic severity of asthma and ranging from 1 to 5 (range: 1 to 4; mean +/- SEM: 2.2 +/- 0.1) and FEV1 (range: 45 to 130 percent; mean +/- SEM: 82 +/- 1.8 percent of predicted values). Bronchoscopy was done in a standardized manner. A first aliquot of 50 ml of saline each were instilled and the BALF recovered was pooled (alveolar sample). After centrifugation, total and differential cell counts (May Grünwald-Giemsa) were carried out on bronchial and alveolar samples. RESULTS: The alveolar sample contained significantly more cells per milliliter of BALF than the bronchial sample in normal (p less than 0.0077, Wilcoxon test) and in asthmatic subjects (p = 0.0001, Wilcoxon test). Both in normal and asthmatic subjects, bronchial samples contained significantly more neutrophils and epithelial cells and fewer macrophages and lymphocytes than alveolar samples. In asthmatic subjects, the bronchial sample contained a significantly greater percentage of eosinophils than the alveolar sample. Eosinophils were significantly increased in asthmatic subjects for both the bronchial and alveolar samples. Bronchial and alveolar eosinophilia both were correlated with the Aas score (r = 0.25, p = 0.024 and r = 0.38, p = 0.0006, respectively, by Spearman Rank test). CONCLUSIONS: This study shows in a large number of subjects that the cell content of bronchial and more distal segments of the lung is not comparable, indicating that studies should not give pooled data in asthmatic subjects. Moreover, it confirms the presence of BALF eosinophilia in asthmatic subjects.

Adolescent↗
PubMed1992

Airway macrophages releasability in bronchial asthma.

Asthma is a multifactorial disease on genetic basis. Its development is influenced by maternal and environmental factors, i.e. allergens and adjuvants. Early identification of candidates at high risk for development of asthma will enable giving recommendations on preventive measures focussing on exposure to tobacco smoke and other pollutants, indoor and outdoor allergens and possibly viral infections during infancy.

Asthma↗
PubMed1991

Indirect evidence of bronchial inflammation assessed by titration of inflammatory mediators in BAL fluid of patients with asthma.

Bronchial inflammation is a characteristic of asthma that may be examined indirectly by bronchoalveolar lavage (BAL). Nine normal individuals were compared with 38 age-matched adults with asthma of variable severity to appreciate the importance of cell activation in the severity of asthma. The severity of asthma was appreciated by the clinical score of Aas and the pulmonary function of the patients. FEV1 ranged between 35% and 130% of predicted. The indirect activation of eosinophils (EOSs), mast cells, fibroblasts, and neutrophils was examined by the titration of eosinophil cationic protein (ECP), tryptase, hyaluronan (HA), and myeloperoxidase (MPO) by radioimmunoassay in BAL fluid (BALF) and cytology of BALF. In the adults with asthma, there was a significantly increased number of EOSs and a significantly increased level of all mediators but MPO. MPO levels were increased in seven patients only; three of these patients were previous smokers. Only ECP and HA levels were significantly correlated with the severity of asthma. These results demonstrate EOSs, mast cells, and fibroblasts are activated in asthma, whereas the involvement of neutrophils is less clear. There was a significant correlation between ECP and HA levels, suggesting a common activation of EOSs and fibroblasts.

Adult↗
PubMed1991

Inflammatory processes in asthma.

Bronchial inflammation is a characteristic of asthma, but, although postmortem and rare bronchoscopic studies had been performed, it is only after 1980 that many experiments were done. Electron microscopy, immunohistochemistry and molecular biology have enhanced our knowledge. As bronchial biopsies and bronchoalveolar lavage present drawbacks, it is favorable to combine both to obtain the best insights into inflammation. The epithelium is rarely intact in asthmatic patients, the cells being both 'fragile' and activated. Eosinophil inflammation is highly important and likely involved in the damage of the epithelium and submucosa. Airway macrophages and monocytes are present in greater amounts and are activated in the bronchi, and they are certainly involved in the pathogenesis of asthma. Mast cells are activated and some emphasis has been put on lymphocytes. Therefore, asthma appears to be a desquamative bronchitis with mixed cell infiltrate.

Acute Disease↗
PubMed1991

[An unusual miliary pattern].

Syndromes presenting with interstitial radiological signs are often difficult to diagnose aetiologically. Surgical biopsy prevents certain rare cases being neglected notably when there are atypical manifestations. We describe a case of bronchiolitis obliterans with an organising pneumonia which was classical as regards the histology and its response to treatment but unusual as regards the clinical presentation and the aetiology.

Adult↗
PubMed1991

[Bronchial inflammation in asthma. Evaluation by bronchial biopsies].

Our understanding of the pathogenesis of asthma has benefitted as a result of bronchial endoscopic techniques linked to studies of bronchoalveolar lavage (LBA) and bronchial biopsy. By using modern biochemical and immunohistochemical methods as well as ultrastructural studies we are better able to specify the importance of bronchial inflammation. Currently we underline the role of epithelial lesions and of intraepithelial lesions and sub-basal inflammation. The responsibility of eosinophils in the epithelial disorder has been proved in vivo by the evidence of cationic protein found both in the LBA liquid and by the tissue localisation thanks to immunological markers. An understanding of the infiltrates and of the state of cellular activation in situ constitutes an initial step in the comprehensive of inflammation; however, these studies do not yet allow us to fully understand the mechanisms of regulation and also the trigger factor in cellular dysfunction which may be the cause. The pseudo-thickening of the basal membrane and sub-epithelial fibrosis are poorly understood, but is probably involved in epithelial repair. The histopathological mechanisms which underly the bronchial aging are equally poorly understood. In the future a better understanding of these problems of neuro-inflammatory disturbances and of epithelial permeability should facilitate the therapeutic approach.

Asthma↗
PubMed1990

Eosinophilic inflammation in asthma.

BACKGROUND AND METHODS: The importance of eosinophils in the pathogenesis of bronchial asthma is not established. In an attempt to evaluate the role of eosinophilic inflammation in asthma, we compared 10 normal subjects with 43 patients with chronic asthma, 19 of whom had severe disease as assessed by a clinical scoring method described by Aas and by pulmonary-function tests. Eosinophils were counted in peripheral blood and bronchoalveolar-lavage fluid, and in biopsy specimens obtained from the patients and post mortem from 8 subjects without asthma, but not from the 10 normal controls. Eosinophil cationic protein was titrated by radioimmunoassay in the bronchoalveolar-lavage fluid from all subjects and studied by immunohistochemistry in the biopsy specimens. RESULTS: There was a significant increase in the number of peripheral-blood eosinophils in the patients that was correlated with the clinical severity of asthma (P less than 0.001) and pulmonary function (P less than 0.03). Levels of eosinophils and eosinophil cationic protein were increased in the bronchoalveolar-lavage fluid from the patients and were also correlated with the severity of asthma (P less than 0.001 and P less than 0.002, respectively). Hematoxylin-eosin staining of bronchial-biopsy specimens showed that intraepithelial eosinophils were present only in patients with asthma. Immunohistochemical analysis of eosinophil cationic protein revealed that normal subjects had only a few nondegranulated eosinophils deep in the submucosa, whereas all the patients had degranulated eosinophils beneath the basement membrane and among epithelial cells. In some patients there was a relation between the presence of degranulated eosinophils and epithelial damage. CONCLUSIONS: Eosinophilic inflammation of the airways is correlated with the severity of asthma. These cells are likely to play a part in the epithelial damage seen in this disease.

Adult↗