Résumé
Objective To understand the distribution of pathogenic genes in uropathogenic Esche-richia coli (UPEC) from urinary specimen and to analyze the pathogenicity of UPEC and their mechanism of apoptosis to HeLa cells. Methods We have analyzed 6 pathogenic genes among the 28 strains of the clini-cally isolated E. coli from urinary tract infected patients. The 6 pathogenic genes were surveyed by using the PCR amplification of the target genes. The adhesion experiments and tryphan-blue staining was used to screen the phenotype of the pathogenic strains, while Annexin V/PI method was applied to study the strains to cause apoptosis of the HeLa cells, which was further confirmed with electronic microscopy. Results We have detected 6 strains that carried the usp gene. Phenotype screening identified two high virulent isolates (strain 6N and 27N) from the 6 strains. Strain 27N and 6N contained very similar virulence gene profile ex-cept that strain 27N did not contain usp gene. Both strains can destroy HeLa cell within 3 hours causing cell death. Results of apoptosis detected by flow cytometry revealed that strain 6N induced 20.75% of HeLa cells to an early stage apoptosis within 1.5 hours. On the other hand, strain 27N induced only 1.55% of HeLa cells to apeptosis. Conclusion High virulent UPEC strain carrying usp gene can induce HeLa cell rapid early apoptosis.
Résumé
Fibronectin (FN) is a major extracellular matrix glycoprotein, highly expressed in developing rat lungs. Several observations suggest that it play an important role in many developmental processes of animals. In vitro, FN can affect the adhesion, migration, proliferation, differentiation, and even apoptosis of various cell types. This study was undertaken to describe the distribution and localizations of fibronectin in the alveolar septum of lungs and liver lobules after CS gas exposure to experimental rats. The experimental rats (Sprague-Dawley strain), weighing 150~200 gm were sacrificed at 6 hours, 12 hours, 24 hours, 48 hours and 72 hours after CS gas exposure. The specimens of lung and liver were prepared for fibronectin immunoreactions of alveolar septa and liver lobules on experimental group, and for fibronectin reactions on the cytoplasm of type I alveolar cells, type II alveolar cells, fibroblasts, alveolar macrophages and interstitium in alveolar septa of lungs. All of specimens for immune reactions were observed with light and electron microscopes. The results obtained were as follows. 1. The liver lobules showed mild fibronectin reactions at the 6 hours and 12 hours after CS gas exposure. 2. The alveolar macrophages revealed strong fibronectin reactions. But alveolar septa showed weak FN reactions at 6 hours after CS gas exposure. 3. At 12 hours and 24 hours after CS gas exposure, the interstitial pneumonitis were seen in the lung alveoli. The gold particles were increased in the cells of alveolar septa, weak fibronectin reactions were revealed in the alveolar septum. 4. At 48 hours and 72 hours after CS gas exposure, FN reactions of alveolar septa were moderate, and the gold particles in the alveolar cells were markedly decreased. These results suggest that CS gas exposure to rats induces the increase of the fibronectin in lung and liver.