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Biomedical subjects

M T Chambe

Publications and source records attributed to M T Chambe.

6 recordsLinked to original sources
PubMed2002

In vitro expression of fas and CD40 and induction of apoptosis in human cystic fibrosis airway epithelial cells.

Cystic fibrosis is characterized by a damaged airway epithelium with inflammation and chronic infection. The aim of this study was to investigate the process of apoptosis in this disease. To evaluate the effects of interferon gamma and the Fas apoptotic pathway on cystic fibrosis airway epithelial cells, we used immortalized cystic fibrosis (CFT-1 and CFT-2) and normal (NT-1) human tracheal epithelial cell lines. Cell death was determined usingannexin-V/propidium iodide labelling and electron microscopy. In vitro expression of Fas and CD40 surface antigens was analysed by immunofluorescence staining and flow cytometry. Normal and cystic fibrosis cells constitutively express these antigens. CD40, but not Fas expression, was upregulated by interferon gamma. Treatment of interferon gamma-stimulated cells with anti-Fas resulted in apoptosis for about 80% of CFT-2 (homozygous for delta F508 deletion) cells and for 35-40% of CFT-1 (heterozygous) or normal cells. Our results suggest that Fas may mediate apoptosis in cystic fibrosis airway epithelium.

Antibodies, Monoclonal↗
PubMed1999

Fas and Fas ligand expression in cystic fibrosis airway epithelium.

BACKGROUND: Cystic fibrosis (CF) is a genetic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene and defective expression of CFTR protein in epithelial cells. The main cause of mortality in CF is linked to chronic inflammatory and infectious airway processes. Recent studies have suggested perturbations in the apoptotic process in CF cell lines and enterocytes. A study was undertaken to investigate the expression of Fas and Fas ligand (FasL) in CF bronchial epithelium and CF tracheal cell lines. METHODS: Immunohistochemical staining for Fas (alkaline phosphatase anti-alkaline phosphatase) and FasL (immunoperoxidase) was performed in eight CF bronchial epithelial samples and four controls and immunohistochemical DNA fragmentation (TUNEL) was carried out in four CF patients and four controls. Immunofluorescence staining and flow cytometric analysis of Fas and FasL expression was performed in two human tracheal epithelial cell lines (HTEC) with normal and CF genotype. The dosage of serum soluble FasL was examined in 21 patients with CF and 14 healthy volunteers. RESULTS: FasL expression was markedly increased in patients with CF in both the ciliated and submucosal glandular bronchial epithelium compared with controls; Fas was similarly expressed in bronchial samples from controls and CF patients in both the ciliated epithelium and submucosal glands. High levels of DNA fragmentation were observed in CF but with some epithelial cell alterations. Serum concentrations of soluble FasL were frequently undetectable in patients with CF. In vitro, HTEC expressed Fas and FasL in both genotypes. A higher mean fluorescence intensity for FasL expression was noted in CF genotype HTEC with median (range) for six experiments of 74 (25-101) for CF cells and 42 (21-70) for non-CF cells. CONCLUSION: Fas/FasL interaction is probably implicated in the human CF airway apoptotic pathway. The mechanisms of induction of FasL expression and its role in inducing tissue damage or remodelling or in controlling local inflammatory cell apoptosis remain to be determined.

Adolescent↗
PubMed1989

[Challenge provocation tests and non-specific bronchial hyperactivity in occupational asthma].

The aim of the study is to determine the interest of realistic challenge (nasal and bronchial) in occupational respiratory symptoms appearing during work. 75 patients were included in the study. The protocol included prick tests, measuring total and specific IgE, spirometry and metacholine test to assess bronchial hyperreactivity (BHR), realistic challenge by rhinomanometry and plethysmography measuring NR (nasal resistance) and RWA (Airway resistance). The test was considered positive if the RWA and/or NR were increased by 100%. 68% of the tests were positives in rhinomanometry and/or plethysmography. There is an BHR in 68% cases of occupational asthma. There is a quite strong correlation between the positivity of the realistic tests and the existence of a non specific BHR.

Asthma↗
PubMed1989

[Challenge provocation tests and nonspecific bronchial hyperreactivity in occupational asthma].

The aim of the study is to determine the interest of realistic challenge (nasal and bronchial) in occupational respiratory symptoms appearing during work. 75 patients were included in the study. The protocol included prick tests, measuring total and specific IgE, spirometry and metacholine test to assess bronchial hyperreactivity (BHR), realistic challenge by rhinomanometry and plethysmography measuring NR (nasal resistance) and RWA (Airway resistance). The test was considered positive if the RWA and/or NR were increased by 100%. 68% of the tests were positives in rhinomanometry and/or plethysmography. There is an BHR in 68% cases of occupational asthma. There is a quite strong correlation between the positivity of the realistic tests and the existence of a non specific BHR.

Asthma↗
PubMed1987

Phosphatidylethanolamine methyltransferase and cAMP, cGMP phosphodiesterases in lymphocytes and monocytes in sarcoidosis.

Among the various hypotheses proposed to explain immune cell defect in sarcoidosis, we examined thoroughly that of Faguet who described abnormalities of signal transmission at lymphocyte membrane level. Phosphatidylethanolamine methyltransferase and cAMP cGMP phosphodiesterases were studied in blood lymphocytes and monocytes from 8 subjects with sarcoidosis disease. Phosphatidylethanolamine methyltransferase (PMT1) plays an important regulatory role in membrane signal transmission. cAMP and cGMP phosphodiesterases (PDE) regulate cytoplasmic cyclic nucleotide levels and so participate in the modulation of the cell cycle. We observed a decreased PMT1 activity in lymphocytes and monocytes and a decreased cAMP and cGMP PDE activities in monocytes. It is not now possible to say if these abnormalities are primary or secondary. Whatever the origin of this dysfunctioning, these results evoke simultaneous disturbances of membrane signal transmission and cell cycle in monocytes and membrane abnormalities in lymphocytes. These abnormalities could explain some immune cell defects in sarcoidosis disease.

3',5'-Cyclic-AMP Phosphodiesterases↗