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Biomedical subjects

Y Sibille

Publications and source records attributed to Y Sibille.

At least 37 records · Page 2Linked to original sources
PubMed1995

Protein content in bronchoalveolar lavage fluid of patients with asthma and control subjects.

BACKGROUND: Secretory component (SC), Clara cell protein (CC10) and to some extent, IgM are proteins locally synthetized in airways. Albumin, alpha 2-macroglobulin and alpha 1-antitrypsin are mainly plasma proteins. In patients with asthma, blood proteins may occur in greater amounts in bronchoalveolar lavage fluid (BALF) than in control subjects because of plasma extravasation. These proteins were measured in BALF to define markers of local synthesis and plasma exudation. METHODS: Twenty-four patients with asthma (mean age, 40 +/- 3.1 years) and 24 control subjects (mean age, 29 +/- 11 years) were tested. Five aliquots of saline solution (50 ml) were instilled, and the recovered BALF was stored. Clara cell protein was measured by a sensitive immunoassay technique based on the agglutination of latex particles. SC, immunoglobulins, alpha 2-macroglobulin, alpha 1-antitrypsin, and albumin were measured by an immunoradiometric assay. Protein concentrations were normalized to albumin. RESULTS: In BALF from patients with asthma there was a significant increase in alpha 2-macroglobulin and IgM and a significant decrease of SC, alpha 1-antitrypsin, and Clara cell protein compared with control subjects. Also, the ratio to albumin was significantly increased for alpha 2-macroglobulin and IgM and decreased for SC. There was no correlation between the severity of asthma and the amount of proteins. CONCLUSIONS: BALF protein content is significantly different in patients with asthma and control subjects, for proteins produced locally and derived from plasma.

Adolescent↗
PubMed1995

Latex gloves with a lower protein content reduce bronchial reactions in subjects with occupational asthma caused by latex.

Latex gloves have been documented as causing rhinitis and asthma. Using inhalation challenges, we evaluated the bronchial response to hypoallergenic gloves in eight health care workers with latex-induced asthma. The subjects were exposed to the powdered latex gloves causing asthma at work and various brands of gloves with a lower protein content, either low-powdered, nonpowdered, or powdered. Exposure to hypoallergenic gloves resulted in the absence (in six subjects) or a significant reduction (in two subjects) of bronchial response. The effects of repeated exposure to hypoallergenic gloves was assessed in two subjects who did not demonstrate changes in peak expiratory flow rates and nonspecific bronchial responsiveness to histamine. This study on a limited number of patients suggests that the use of hypoallergenic gloves could be an effective means of reducing the risk of asthmatic reactions in health care workers with latex-induced asthma when complete avoidance cannot be achieved. The long-term effect of exposure as well as the widespread use of hypoallergenic gloves warrant further investigation on larger cohorts of subjects.

Adult↗
PubMed1995

Potential role of Clara cell protein, an endogenous phospholipase A2 inhibitor, in acute lung injury.

It is now recognized that epithelial cells lining airways and alveoli are capable of releasing various mediators, which have the potential to modulate local inflammatory reactions. The amount of the 16 kDa Clara cell protein (CC16), an inhibitor of phospholipase A2 activity produced by pulmonary epithelial cells, was measured by means of a sensitive immunoassay in the unconcentrated bronchoalveolar lavage fluid (BALF) of 13 control subjects, and in patients with acute lung injury (14 with the full-blown adult respiratory distress syndrome (ARDS); 21 after standard cardiopulmonary bypass surgery, a known risk factor for ARDS). The level of CC16 was compared with other markers of inflammation with a wide range of molecular weights: albumin (nephelometry); total protein (spectrophotometry); beta 2-microglobulin (latex immunoassay); cystatin C (latex immunoassay); alpha 1-antitrypsin (immunoradiometry), and lipocortin-1 (enzyme-linked immunosorbent assay (ELISA)). The Clara cell protein (CC16) was detectable in all BALF, and significantly higher levels of this protein were observed in BALF from patients with acute lung injury. Changes in BALF Clara cell protein levels differed from those of alpha 2-macroglobulin and the natural phospholipase inhibitor lipocortin-1. Alpha 2-macroglobulin levels were not significantly enhanced in patients at risk for ARDS, but were increased in patients with ARDS; whereas, lipocortin 1 levels were not elevated in either group. Pretreatment of patients at risk for ARDS with high dose methylprednisolone did not alter the amount of Clara cell protein recovered in BALF. The mean CC16 level in BALF from patients with ARDS who died was significantly lower than from those who survived. The data presented in this study suggest that pulmonary epithelial cells secrete a natural anti-inflammatory protein during acute lung injury, which might have a protective and immunosuppressive role.

Adult↗
PubMed1995

[Spontaneous pneumothorax. Results of pleural talc therapy using thoracoscopy].

The aim of this retrospective study is to evaluate the advantage of thoracoscopy and the efficacy of talcage in the treatment of spontaneous pneumothorax (SP). Two hundred cases have been analyzed with a follow-up of 1 to 8 years after the occurrence of the disorder. The ratio man/woman is 4/1. One hundred and forty two pneumothorax are considered as being of idiopathic origin and 58 are associated to bronchopneumopathy, with a mean age of 33 and 56 years, respectively. The percentage of smokers is 69.5% with a mean smoking of 14 packets/years. The endoscopic aspect of pleura is either normal (30%) or shows adhesions (23.5%), blebs (17%) or bullaes (29.5%). Thoracoscopy allowed talc poudrage in 191 patients and allowed to indicate the need for surgery in nine patients. The immediate success rate of talcage is 93.7%. In the group of immediate failure (6.3%), unexpected bullous structures (8/12) are found at tomodensitometry (TDM), as well as during surgery. Late recurrence is reported in 2 cases (1%) at 20 and 25 months. Radiological sequelaes are minimum (9%). Lung function testing in patients with idiopathic pneumothorax (n = 64) shows, before talc poudrage, signs of pulmonary hyperdistension (total lung capacity (TLC) at 116% of predicted values), reflecting the illness pathology, 3 months after talcage a discrete restrictive syndrome (TLC 93%) and one year after the partial recovery of the lost volume (TLC 105%). Tomodensitometry revealed to be complementary to thoracoscopy in secondary SP and very instructive in idiopathic SP after immediate failure of talc poudrage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Validation of IgA1 and IgA2 measurements by a solid-phase immunoradiometric assay in serum and secretions.

We describe specific, sensitive and reproducible immunoradiometric assays to measure total IgA and IgA subclass levels in biological fluids, which take into account the problem that polymeric forms are differently recognized in immunoassays. Sera from subjects totally deficient in one of the IgA subclasses allowed us to ensure the specificity of the subclass assays and to define the proportions of IgA1 (84%) and IgA2 (16%) in the normal pooled serum (from 30 blood donors) used as standard. With purified milk 11-S secretory IgA1 and 11-S secretory IgA2, we determined a correction factor for the corresponding polymeric forms using, respectively, monomeric IgA1 and monomeric IgA2 from pooled serum as standards. With the monoclonal antibodies used, purified 11-S secretory IgA1 was similarly recognized by both the total IgA assay and the IgA1 assay; both total IgA and IgA1 concentrations were underestimated compared with monomeric IgA or monomeric IgA1. In contrast, 11-S secretory IgA2 was better recognized by the IgA2 assay than by the total IgA assay and the values were thus overestimates. Considering this problem of recognition, we fractionated saliva and lung secretions by sucrose density gradient ultracentrifugation before measuring their IgA1 and IgA2 levels.

Adult↗
PubMed1994

Bronchoalveolar lavage immunoglobulin A and G and antiproteases correlate with changes in diffusion indices during the natural course of pulmonary sarcoidosis.

We wanted to determine whether cell populations and soluble components in bronchoalveolar lavage (BAL) could be useful in predicting the outcome of lung function and chest radiography in patients with untreated pulmonary sarcoidosis. Analysis of soluble proteins in BAL fluid, included the levels of immunoglobulins and the two major antiproteases, alpha 2-macroglobulin (alpha 2-M) and alpha 1-protease inhibitor (alpha 1-PI), expressed as a relative coefficient of excretion (RCE). Thirty one nonsmoking patients with biopsy proven sarcoidosis, who remained untreated, had reassessment of lung function tests after 6-54 months (median 21 months). No correlation was observed between initial BAL data and changes in lung volumes and radiographic opacities. By contrast, the initial BAL immunoglobulin A and G (IgA and IgG) RCE correlated inversely with the change in transfer factor for carbon monoxide (TLCO) in the whole group and in patients with sarcoidosis of recent origin (estimated disease duration < 6 months). In the whole group and in patients with longstanding disease (estimated disease duration > 24 months, or radiographic Stage 4), the change in carbon monoxide transfer coefficient (KCO) correlated negatively with the initial alpha 1-PI RCE and positively with the initial helper to suppressor T-cell (T4/T8) ratio. By contrast, no significant difference in BAL cellular and protein data was found between patients with recent and longstanding sarcoidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Fc alpha-receptor expression on the myelomonocytic cell line THP-1: comparison with human alveolar macrophages.

Immunoglobulin A (IgA) and alveolar macrophages are two important components of the immune system in the respiratory tract. Fc alpha-receptors (Fc alpha R) are present on neutrophils, eosinophils and a series of human mononuclear phagocytes, including monocytes, alveolar macrophages and leukaemia cell lines (U-937). In the present study, using idiotypes and anti-idiotypic antibodies, we report that THP-1 cells, a myelomonocytic cell line, constitutively express Fc alpha R and that all IgA preparations used bind the receptor. Of the stimuli used (phorbol myristate acetate, retinoic acid, calcitriol), only calcitriol can induce differentiation of THP-1 cells, as assessed by CD14 expression. The expression of Fc alpha R appears to be independent of cell differentiation, since calcitriol pretreatment has no effect on IgA-binding. Finally, My43, a monoclonal antibody recognizing the Fc alpha R on U-937 cells, does not bind to THP-1 cells or to human alveolar macrophages. In addition, preincubation of THP-1 cells or human alveolar macrophages with My43 does not diminish IgA-binding to these cells. Ribonucleic acid (RNA) encoding the Fc alpha R isolated from U-937 is expressed, although possibly at a lower level, in alveolar macrophages and THP-1 cells. In conclusion, Fc alpha R are constitutively expressed on THP-1 cells and share some characteristics with the Fc alpha R described in human alveolar macrophages. THP-1 cells, therefore, may represent a reasonable model for further investigation of the interaction of immunoglobulin A and tissue macrophages.

Base Sequence↗
PubMed1993

Pulmonary immune cells in health and disease: polymorphonuclear neutrophils.

The pulmonary vasculature represents the largest reservoir of polymorphonuclear neutrophils (PMNs) in the human body. This is in striking contrast with the paucity of PMNs present in the normal airways and alveoli. However, the respiratory tract constitutes an easy access for microorganisms and particles present in inhaled air and, therefore, efficacious defence mechanisms are required. When the mucociliary clearance and the alveolar macrophages are over-whelmed, the rapid recruitment of PMNs from the lung vasculature appears to be a crucial response of the host against the pathogens. The regulation of adherence of PMNs to endothelial cells (EC), followed by the transendothelial migration are now better understood, and are under the control of a series of adhesion molecules modulated by bacterial and inflammatory mediators. In addition to their defensive role, PMNs have also been implicated in acute and chronic injurious diseases of the lung. Clearly, PMNs contain enough cytotoxic and proteolytic material to induce lesional changes. However, the release of this material is likely to be dependent on environmental factors, including mediators derived from other inflammatory and immune cells. The presence or absence of these factors could explain the fact that high numbers of PMNs can be observed in the airways and alveoli without major lesions whilst in other conditions, a marginal increase of PMNs in the respiratory tract can be associated with major damage and irreversible architectural changes in the lung.

Cell Adhesion Molecules↗
PubMed1992

Bronchoalveolar lavage in alcoholic liver cirrhosis. T-lymphocyte subsets and immunoglobulin concentrations.

The purpose of this study was to determine the phenotype profiles of immune effector cells and the concentrations of immunoglobulins in the lower respiratory tract of non-smoking patients with alcoholic liver cirrhosis (ALC). Nine nonsmoking patients with liver biopsy-proved ALC (grade B or C cirrhosis in Child's classification), free of clinical pulmonary symptoms, and with normal chest roentgenogram were included in the study. The control group included 12 healthy nonsmokers. Each patient had fiberoptic bronchoscopy with bronchoalveolar lavage (BAL). The number of T cells and of lymphocyte subpopulations was determined by immunofluorescence studies using monoclonal antibodies that were specific for CD3, CD4, and CD8 markers. Patients with ALC exhibited a dramatically increased percentage of CD8+ cells in BAL that induced a low CD4/CD8 ratio (0.96 +/- 0.15 vs 1.8 +/- 0.12 in healthy controls). Further characterization of lymphocyte subsets' dual immunofluorescence analysis demonstrated that most of the CD8+ alveolar lymphocytes had a phenotype of cytotoxic cells (CD8+ CD11b-; 48 percent +/- 13 in ALC vs 10 percent +/- 5 in controls). ALC was associated with an appreciable alveolar-capillary "leak" as demonstrated by a significant increase in BAL fluid albumin. In addition, the concentrations of immunoglobulins in BAL fluid were significantly greater in ALC than in controls. However, the relative (to albumin) coefficient of excretion of IgG, A, and M in and alpha 2-macroglobulin BAL fluid was not significantly different between controls and ALC. Our results indicate that increased proportions of CB8+ and especially of CD8+ CD11b- cells are a common feature in the lower respiratory tract of nonsmoking patients with ALC. These changes may be of potential functional importance in the regulation of the local pulmonary immune response in ALC.

Adult↗
PubMed1992

Clara cell protein in serum and bronchoalveolar lavage.

The 10 kDa Clara cell protein was measured in serum and bronchoalveolar lavage (BAL) from 39 healthy subjects (14 smokers, 25 nonsmokers) and from 41 patients with respiratory disease (chronic obstructive pulmonary disease (COPD), sarcoidosis, lung cancer). Clara cell protein appears as one of the most abundant respiratory tract derived proteins, with values averaging 7% of the total protein content of lung lavages from healthy nonsmokers. A significant reduction of Clara cell protein was found in BAL from smokers and patients with COPD or lung cancer. The same pattern of change was found in the concentrations of Clara cell protein in serum. Pulmonary sarcoidosis did not affect absolute values of Clara cell protein in lung lavages but was associated with elevated levels in serum. Changes in lung lavage Clara cell protein differed from that of albumin, beta 2-microglobulin or the secretory component, since the latter were unaffected by smoking or COPD but increased in sarcoidosis and lung cancer. These results indicate that Clara cell protein in BAL or serum might serve as a sensitive indicator of nonciliated bronchial cell dysfunction.

Adult↗
PubMed1991

Isolation of an inhibitor of neutrophil function from bronchial lavage of normal volunteers.

Bronchial inflammation is associated with a reduction in airway caliber. Factors that may dampen this inflammation are ill defined. We have developed a model of airway inflammation using an extract of cotton bracts (CBE). In the current study we characterize inhibitor(s) of polymorphonuclear neutrophil (PMN) function in bronchial lavage (BL) fluid and examine the relationship between inhibitor concentrations and induction of bronchial inflammation or bronchoconstriction by CBE. We report that BL obtained contains factors that inhibit PMN hydrogen peroxide production and chemotaxis to formylmethionylleucyl-phenylalanine (FMLP). In two different subject populations the relative degree of a one molecular mass inhibitor was greatest in BL from subjects that manifested little bronchoconstriction to CBE compared with other subjects. In one subject population the relative amount of this inhibitor correlated inversely with the bronchoconstricting response to CBE and a number of parameters of airway inflammation including PMN noted on bronchial biopsy after CBE instillation. Partial chemical characterization of one molecular mass BL-derived inhibitor reveals it is of low molecular mass (less than 1,000 Da), nonpolar, and sensitive to aminopeptidase digestion. The finding that the bronchial environment contains variable concentrations of an oligopeptide that inhibits PMN function has important implications for treatment of inflammatory airway diseases.

Aminopeptidases↗
PubMed1991

IgA triggers tumor necrosis factor alpha secretion by monocytes: a study in normal subjects and patients with alcoholic cirrhosis.

Under endotoxin-free conditions, peripheral blood mononuclear cells and purified monocytes isolated from healthy control subjects and patients with alcoholic cirrhosis disclose elevated tumor necrosis factor alpha messenger RNA level and produce tumor necrosis factor alpha in response to stimulation by either soluble polymeric IgA or monomeric IgA bound to the surface of culture dishes but not by soluble monomeric IgA. Polymeric IgA induces tumor necrosis factor alpha secretion in a dose-dependent fashion. These results suggest that cross-linking of Fc alpha receptors on human monocytes induces the messenger RNA accumulation and the secretion of the cytotoxic and immunoregulatory cytokine tumor necrosis factor alpha. Furthermore, it is shown that lipopolysaccharide-induced tumor necrosis factor alpha secretion by peripheral blood mononuclear cells is synergistically enhanced in the presence of solid phase monomeric IgA but not in the presence of either soluble monomeric or polymeric IgA. Although increased lipopolysaccharide-induced tumor necrosis factor alpha secretion is observed at baseline in alcoholic cirrhotic patients, this synergism is also expressed in this group of patients. These observations could be of pathophysiological relevance in alcoholic cirrhosis because monomeric IgA deposits along the liver sinusoids and increased serum levels of polymeric IgA are common even in the early stages of this disease.

Female↗
PubMed1990

Macrophages and polymorphonuclear neutrophils in lung defense and injury.

Phagocytes, in particular macrophages and PMN, are now recognized as major components of inflammatory and immunologic reactions in the lung. Normally, macrophages represent the majority of phagocytes in the lower respiratory tract. These lung macrophages are morphologically and functionally heterogenous and include alveolar, interstitial, intravascular, and airway macrophages, each with characteristic morphologic and functional features. Through the presence of surface receptors for numerous ligands and through their large number of secretory products, lung macrophages can respond to environmental factors and account for most of the clearance of microparticles and microorganisms in the distal airways and the alveolar spaces. In addition, macrophages also play an important role in inflammatory processes through the release of oxygen radicals and proteolytic enzymes. Through the release of several cytokines, i.e., growth-promoting and inhibiting factors, lung macrophages may also influence both matrix damage and repair processes. Macrophages can also contribute to the alveolitis by recruitment of inflammatory and immune cells. This latter contribution is best demonstrated in migration movement of PMN. The normal distal airways generally contain a small number of PMN, but the pulmonary vascular bed represents a large reservoir of PMN. Some of them are in intimate contact with the endothelium, forming the so-called marginating pool of PMN. Because the capillary lumen is separated only from the alveolar space by a monolayer of endothelial and epithelial cells on each side of a thin interstitial matrix, it is likely that some inhibitory mechanism exists to prevent PMN from migrating towards the alveolar space. Such inhibitors of PMN migration are present both in serum and in the alveolar space, some being released by alveolar macrophages. However, alveolar macrophages can also secrete factors called chemotaxins that attract PMN to the airways, and this supports a central role for alveolar macrophages in the regulation of PMN traffic in the lungs. Thus, secretory products of alveolar macrophages are part of the regulatory mechanisms of PMN mobility and adherence that appears to be crucial in the initiation of some inflammatory reactions. The contribution of phagocytes to the defense against infection and tumor has been documented mostly in vitro. Thus, both oxygen radicals, in particular hydroxyl radicals and proteases such as lysozyme, are potent bactericidal agents. That phagocytes are also important defenders of the lungs in vivo is best supported by the observations in immunodeficient patients and animal models.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Phagocyte enzymes in bronchoalveolar lavage from patients with pulmonary sarcoidosis and collagen vascular disorders.

The balance between proteases and antiproteases in the lower respiratory tract is believed to play a role in the outcome of interstitial lung diseases. In this cross-sectional study, we measure several phagocyte derived enzymes, namely plasminogen activator, neutrophil elastase and an ill-defined protease active on the trialanine chromophore substrate succinyl-alanine3-nitroanilide (SLAPN) in bronchoalveolar lavage (BAL) fluid from 42 patients with pulmonary sarcoidosis and from 43 patients with collagen vascular disease (CVD), 22 without lung disease (group I) and 21 associated with parenchymal lung disease (group II). The results show: a) that sarcoidosis is associated with increased plasminogen activator activity and with the presence of enzymatic activity against SLAPN corresponding at least in part to a metalloprotease; b) that CVD in the absence of radiographic lung disease is associated with an increase of plasminogen activator activity and increased levels of alpha 1-antiprotease-neutrophil elastase complexes; c) that the majority of untreated CVD (group II) patients have detectable levels of neutrophil elastase activity. These data show that patients with pulmonary sarcoidosis and CVD have different enzymatic profiles in their lower respiratory tract as assessed by BAL. Thus, sarcoidosis (mostly lymphocytic) is associated with enhanced macrophage-derived proteolytic activity in BAL, while CVD patients both with and without lung disease have increased neutrophil counts and neutrophil elastase complexed to alpha 1-protease inhibitor and presumably inactive in BAL. Finally, only BAL from untreated CVD patients with interstitial lung disease contain neutrophil elastase activity. This latter activity could contribute to the lung lesions frequently observed in these disorders.

Adult↗
PubMed1989

Chemotactic properties of rat immunoglobulins and immune complexes.

The effect of rat immunoglobulins and immune complexes on the locomotor function of rat polymorphonuclear leukocytes (PMN) was investigated in vitro. Rat immunoglobulin G1 (IgG1), IgG2a, IgG2b, and IgA monoclonal antibodies specific for the dinitrophenyl hapten were used. Both monomeric and polymeric IgA showed chemotactic activity in a dose-dependent manner. IgG1 and IgG2b also induced a dose-dependent locomotor response of PMN, but the nature of the induced migration was chemokinetic (enhancing random migration). IgG2a was chemotactic and induced maximal migration at a relatively low concentration. IgG1- and IgG2b-immune complexes induced stronger migration than antibody alone; however, IgA- and IgG2a-immune complexes did not. IgA was shown to modify the chemotactic movement of PMN induced by N-formylmethionyl-leucyl-phenylalanine (FMLP). In the presence of both IgA and FMLP in the lower chamber, the migration towards suboptimal concentrations of FMLP was enhanced. By contrast, IgA in the upper chamber decreased migration towards the optimal or higher concentrations of FMLP. These findings suggest that IgA may work synergistically with luminal chemoattractants to mobilize PMN to the locus of infection on the mucosal surface. In addition, the intense activity of IgG2a alone and IgG1- or IgG2b-immune complexes in inducing PMN migration may play an important role in inflammatory processes. The data indicate that immunoglobulins have a direct effect on PMN mobility.

Animals↗