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Bronchial biopsies

Sampson AP, Cowbum AS, Sladek K, et al. (1997) Profound overexpression of leukotriene C4 synthase in bronchial biopsies from aspirin-intolerant asthmatic patients. Int Arch Allergy Immunol. 113, 355-357. [Pg.375]

Bronchial biopsies of subjects with occupational asthma induced by TDI revealed pathologic features such as increased number of inflammatory cells in the airway mucosa and thickening of subepithelial collagen. ... [Pg.684]

Jeffry PK, Wardlaw AJ, Nelson FC, Collins JV, Kay AB Bronchial biopsies in asthma An ultrastructural, quantitative study and correlation with hyperreactivity. Am Rev Respir Dis 1989 140 1745-1753. [Pg.50]

Y6. Ying, S., Meng, Q., Zeibecoglou, K., Robinson, D. S., Macfarlane, A., Humbert, M., and Kay, A. B., Eosinophil chemotactic chemokines (eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4), and C-C chemokine receptor 3 expression in bronchial biopsies from atopic and nonatopic (intrinsic) asthmatics. J. Immunol. 163,6321—6329 (1999). [Pg.46]

Bentley, A.M., Menq, Q., Robinson, D.S., Hamid, Q, Kay, A.B. and Durham, S.R, (1993). Increases in activated T lymphocytes, eosinophils and cytokine messenger RNA for IL-5 and GM-CSF in bronchial biopsies after allergen inhalation challenge in atopic asthmatics. Am. J. Respir. Cell Mol. Biol. 8, 35-42. [Pg.28]

Bradley, B.L., Azzawi, M., Jacobson, M., Assoufi, B., Collins, J.V., Irani, A.A., Schwartz, L.B., Durham, S.R, Jeffery, P.K. and Kay, A.B. (1991). Eosinophils, T-lymphocytes, mast cells, neutrophils and macrophages in bronchial biopsy specimens from atopic subjects with asthma - comparison with biopsy specimens from atopic subjects without asthma and normal control subjects and relationship to bronchial hyperresponsiveness. J. Allergy Chn. Immunol. 88,661-674. [Pg.74]

The bronchial histopathology of patients who have died of asthma shows an intense infiltration of the bronchial mucosa with inflammatory ceUs, particularly eosinophils, macrophages, lymphocytes and to a lesser extent neutrophils. Deposition of eosinophil products in the bronchial epithelium and subepithelium is a particularly prominent feature (Filley etal., 1982). Epithelial denudation, dilatation of blood vessels, mucosal oedema and hypertrophy of both submucosal glands and bronchial smooth muscle are other features. Many of these features of asthma deaths are also observed in milder and well-controlled asthmatics. Elevated numbers of eosinophils, moncytes/macrophages and activated lymphocytes are persistent features observed in bronchial biopsies... [Pg.101]

Montefort, S., Gratziou, C., Goulding, D., Polosa, R., Haskard, D.O., Howarth, P.H., Holgate, S.T. and Carroll, M.P. (1994). Bronchial biopsy evidence fisr leukocyte infiltration and upregulation of leukocyte-endothelial cell adhesion molecules 6 hours after local allergen challenge of sensitized asthmatic airways. J. Clin. Invest. 93, 1411-1421. [Pg.118]

Glynn, A.A. and Michaels, L. (1960). Bronchial biopsy in chronic bronchitis and asthma. Thorax 15, 142-153. [Pg.161]

Identification of activated T lymphocytes and eosinophils in bronchial biopsies in stable atopic asthma. Am. Rev. Respir. Dis. 142, 1407-1413. [Pg.219]

IL-5 is detectable in bronchial biopsies and bronchoalveolar lavage (BAL) fluid of asthmatics (433, 434). Additionally, inhalation of IL-5 by asthmatics has been shown to cause airway hyperresponsiveness (AHR) and an increase in sputum eosinophils (435). [Pg.177]

Sont JK, Ham J, Van Krieken JM, et al Relationship between the inflammatory infiltrate in bronchial biopsy specimens and clinical severity of asthma in patients treated with inhaled steroids. Thorax 1996 51 496-502. [Pg.124]

As far as the prediction of asthma is concerned, eosinophils as well as their mediators (e.g. eosinophil cationic protein, peroxidase and protein X) have been studied in infancy in order to identify individuals who are developing chronic disease. In a Norwegian study cohort, wheezing infants had significantly higher levels of serum eosinophil cationic protein compared to controls [18(11)]. Whether concentrations of mediators from eosinophils also predict the chronic disease process remains to be shown. Studies of eosinophils in bronchial biopsies have suggested that increased numbers of eosinophils are risk factors for chronic asthma [19(11)]. So far, none of the various immunological markers has been found suitable for the prediction of atopy or asthma on an individual level. [Pg.132]

The major characteristics of asthma include a variable degree of airflow obstruction (related to bronchospasm, edema, and hypersecretion), BHR, and airways inflammation (Fig. 26-1). Evidence of inflammation arose from the studies of nonspecific BEIR, bron-choalveolar lavage (BAL), bronchial biopsies, and induced sputum, as well as from postmortem observations of patients with asthma who died from an attack of asthma or from other causes. To understand the pathogenetic mechanisms that underlie the many variants of asthma, it is critical to identify factors that initiate, intensify, and modulate the inflammatory response of the airways and to determine how these immunologic and biologic processes produce the characteristic airways abnormalities. Immune responses mediated by IgE antibodies are of foremost importance. [Pg.505]

After CSR, a further step leads to the expression of IgE, for the B cells must undergo differentiation into IgE-secreting plasma cells. The co-localization of e-chain mRNA with B-cell-specific markers by dual immunohistochemistry and in situ hybridization in the nasal biopsies of rhinitics and bronchial biopsies from asthmatics indicates that this is highly likely [103-106], and the same conclusion also emerges from assays for IgE protein and IgE protein synthesis. [Pg.127]

Snow RE, Djukanovic R, Stevenson FK Analysis of immunoglobulin E VH transcripts in a bronchial biopsy of an asthmatic patients confirms bias towards VH5, and indicates local clonal expansion, somatic mutation and isotype switch events. Immunology 1999 98 646-651. [Pg.135]

AZZAWI, M BRADLEY, B JEFFREY, P.K., FREW, A.J., WARDLAW, A.J., KNOWLES, G ASSOUFI, B COLLINS, J.V., DURHAM, S. KAY, A.B. (1990) Identification of activated T lymphocytes and eosinophils in bronchial biopsies in stable atopic asthma. American Review of Respiratory Disease, 142, 1407-1413. [Pg.22]

HAMID, Q AZZAWI, M YING, S MOQBEL, R WARDLAW, A.J., CORRIGAN, C.J., BRADLEY, B DURHAM, S.R., COLLINS, J.V. JEFFERY, P. K. (1991) Expression of mRNA for interleukin-5 in mucosal bronchial biopsies from asthmatics. Journal of Clinical Investigation, 87, 1541-1546. [Pg.24]

This observation was further expanded upon by Pelosi and colleagues who observed seven patients with typical or atypical carcinoid tumors that were overdiagnosed as small cell lung cancers in bronchial biopsy specimens. The authors studied bronchial biopsies from 9 consecutive small cell lung carcinoma patients, histologically and immunohistochemically (cytokeratins. [Pg.406]

Consistent with an important role of PDF4 in obstructive lung disease, selective PDF4 inhibitors have been evaluated in clinical trials for the treatment of asthma and COPD. In one study, cilomilast (Ariflo, 15 mg twice daily for 10 weeks) decreased inflammatory cell infiltration sigifificantly in bronchial biopsies of patients with COPD. Further studies are needed to define the role of PDF4 inhibitors in asthma and COPD, but these drugs are promising candidates for new approaches to asthma therapy. [Pg.218]

B.J. Venmans, J.C. van der Linden, G. Sutedja, et al. (2000). Observer variability in histopathological reporting of bronchial biopsy specimens influence on the results of AFB in detection of bronchial neoplasia. J. of BronchoL, 7, 210-214. [Pg.173]


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See also in sourсe #XX -- [ Pg.203 ]




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