摘要:

Bronchial epithelial cells may be involved in the pathogenesis of asthma releasing several inflammatory mediators such as interleukins and lipoxygenase products. In this study we evaluated the spontaneous and A23128‐induced release of IS‐HETE, PGE2 and fibronectin as well as the spontaneous expression of HLA‐DR and ICAM‐1 molecules by bronchial epithelial cells obtained by bronchial brushing from 35 asthmatic and 27 normal subjects. The release of fibronectin and 15‐HETE was studied using the EIA and RIA techniques. The expression of HLA‐DR and ICAM‐1 molecules was studied using the APAAP and the immunofluorescence methods. Bronchial epithelial cells from asthmatics released higher amounts of IS‐HETE and fibronectin both spontaneously (p<0.002, p<0.05, respectively) or after stimulation with calcium ionophore compared with normals. On the other hand, PGE2 release was significantly higher only after stimulation with calcium ionophore (p<0.002). The spontaneous expression of HLA‐DR and ICAM‐1 (p<0.001) was significantly higher on epithelial cells from asthmatics than in normal subjects. Finally, the severity of asthma significantly correlated with the release of LS‐HETE (p<0.02) and the expression of HLA‐DR and ICAM‐ I respectively (p<0.001 and p<0.002, respectively). This study indicates that bronchial epithelial cells are in an activated state in asthma and that the degree of activation is correlated to th

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04696.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04726.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04755.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04697.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04727.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04698.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04756.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

SummaryThe increased knowledge of mucosal cellular events and their regulation within the airways in asthma has been made possible both by the feasibility of direct airway sampling in this disorder by endobronchial biopsy and lavage, and on account of the major advances that have been made in the understanding of the immunological mechanisms involved in inflammation. The appreciation that cell damage and remodelling can arise as a consequence of this inflammation has provided a mechanism whereby the structural abnormalities in asthma may arise. Eosinophil products, such as MBP and ECP, have been shown to be cytotoxic and their release within the epithelium could contribute to damage to this cell population. In addition, collagenases from activated eosinophils, will damage the basement membrane and mast cell derived proteases may loosen intercellular adhesion, both factors which could contribute to epithelial fragility. This epithelial disruption is likely to contribute to bronchial hyperresponsiveness as several reports exist relating epithelial damage to the level of bronchial responsiveness in asthma (53–55) and the epithelium, in addition to generating cytokines, can synthesize bronchodilator substances such as PGE2 and NO, has the capacity to metabolize the bronchoconstrictor SP, through generation of neutral endopeptidases, and contains afferent sensory neurones whose stimulation may be increased in the presence of a disrupted epithelial layer. The deposition of collagen (types III and IV) associated with an increase in tissue myofibroblasts, may reflect an attempt at a repair process (56, 57). This will lead to an increase in airway bulk as will smooth muscle hyperplasia and hypertrophy, both factors which through geometric considerations are likely to contribute to bronchial hyperresponsiveness. Growth factors associated with mast cell, eosinophil and macrophage activation can all be theoretically linked with fibroblast proliferation and activation and smooth muscle mutagenesis. The reduction in mucosal inflammation with corticosteroid therapy in association with improvements in spirometry and bronchial responsiveness (58) provides further support for the inflammatory pathogenesis of the asthma diseas

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04699.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

The plant lectin concanavalin A (Con A) has been shown to induce basophil histamine release by an IgE‐receptor‐dependent process resembling that of anti‐IgE‐antibodies.In this study, the concentration‐response for basophil histamine release from washed blood cells was analyzed in a population of blood samples from adults with a total plasma IgE content ranging from18000 kU/l (n= 108), as well as 148 cord blood samples.The concentration‐response‐curves for anti‐IgE in all adult blood samples were similar, despite the large variation in total plasma IgE ‐ only the cord blood samples showed a decreased sensitivity. In contrast, the optimal concentration of Con A was inversely related to plasma IgE, and this relation was most pronounced in the adult blood samples.It is proposed that IgE‐receptor‐mediated histamine release may be dependent not only on the number of stimulatory, dimeric cross‐links formed between IgE‐receptors, but also on the molecular structure o

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb02175.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0105-4538    

DOI:10.1111/j.1398-9995.1993.tb04757.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY