Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six patients with asthma (American Thoracic Society (ATS) criteria), maintained on inhaled beta 2-agonists alone, were treated with inhaled corticosteroid (budesonide 400 micrograms b.d.) for a period of three months. Prior to steroid therapy, baseline spirometry, bronchodilator response and bronchial hyperresponsiveness were documented and endobronchial biopsies were obtained for immunopathological analysis. Frozen sections of the biopsies were investigated using immunoperoxidase methods, with a panel of monoclonal antibodies selected to reveal the presence and distribution of lymphocyte and macrophage subsets and HLA-DR expression. After three months the studies were repeated. Studies before steroid therapy revealed a T-cell-dominated inflammation in the bronchial wall of all subjects. Baseline airway obstruction, median (range) forced expiratory volume in one second (FEV1) 78.5 (61-109)% of predicted, with a significant bronchodilator response 20.8 (14-33)% and bronchial hyperresponsiveness to histamine geometric mean (SD) PC20FEV1 0.69 (2.5) mg was documented. Steroid therapy caused a significant reduction in bronchial hyperresponsiveness to histamine, with an increase in geometric mean PC20FEV1 to 2.22 (3.2) mg post steroid (p less than 0.03). Concurrent with a reduction in bronchodilator response and an increase in spirometric variables (improved forced midexpiratory flow (FEF25-75) p less than 0.03), there were marked reductions observed in the overall numbers of T-lymphocytes (CD 2, 5, 8), the numbers of CD45RO+ T-cells, and the numbers of macrophages (RFD1+) with the phenotype of antigen presenting cells. In all six subjects, reductions in the quantitative expression of HLA-DR molecules were also seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lung function and immunopathological changes after inhaled corticosteroid therapy in asthma. 157 53

Thoracic duct drainage (TDD) with reinfusion of cell-free lymph was performed in 118 prospective recipients within four months before transplantation. TDD was unsuccessful in 27 patients (A); it yielded 1-19 X 10(9) lymphocytes in 25 cases (B) and 20-185 X -10(9) in 66 cases (C). The incidence of acute rejection episodes and the requirement for early post-transplant dialysis were lower in C than in A. Six patients were studied for T-lymphocyte subsets, using monoclonal antibodies from OKT series and a monomorphic and HLA-DR (BL2) raised in our laboratory. During TDD peripheral blood lymphocyte (PBL) counts decreased and the percentage of BL2 cells increased. Simultaneously, typical small PBL were replaced by large less differentiated cells slightly labelled by OKT3, some of them bearing both OKT4 and OKT8 markers. The larger the depletion, the earlier the emergence of immature T-cells. In lymph fluid, lymphocyte counts decreased later than in blood, the proportion of T8+ cells lacking Fc receptors increased with time. Changes in B patients were less than in C. These results support the hypothesis that T-cell subset modifications represent the main immunological change accounting for better allograft prognosis.
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PMID:Improvement of cadaveric renal allograft survival by thoracic duct drainage: relation with T-lymphocyte subset modifications assessed by flow-cytometry. 622 12