Objective： To establish an animal model of P.aeruginosa biofilm associated with chronic pulmonary infection and investigate the pathogenic effects of biofilm. Methods： Experiments in vitro, measuring the MICS, MBCS ...Objective： To establish an animal model of P.aeruginosa biofilm associated with chronic pulmonary infection and investigate the pathogenic effects of biofilm. Methods： Experiments in vitro, measuring the MICS, MBCS of levofloxacin（LFX）, ceftazidime（CAZ） in PAO579 in alginate beads and planktonic PAO579. Rats were challenged with 0.1 ml of PAO579（109CFU/ml） in alginate beads or 0.1 ml of planktonic PAO579（109CFU/ml）, 3,7,14 days after challenging, bacteriological, pathological features were observed. Results： The MICS, MBCS of LFX, CAZ in PAO579 in alginate beads were higher than those in planktonic PAO579 in vitro. CFU/lung in alginate beads group was significantly higher than that in planktonic bacteria group（P = 0.002, P = 0.004, P = 0.002, respectively）; macroscopic lung pathology and the inflammation in alginate beads group were significantly more severe compared to those in planktonic bacteria group in vivo. Conclusion： P.aeruginosa biofilm protected bacterium from killing of antibiotics and might mediate the host immune damage in the lung tissue and made bacterium evade the host immune defense.展开更多
The expression of IL-4 in a rat model of chronic pulmonary infection biofilm formation induced by Pseudomonas aeruginosa was investigated, in which SPF Wister rats were infected via trachea with 0.1 ml P. aeruginosa s...The expression of IL-4 in a rat model of chronic pulmonary infection biofilm formation induced by Pseudomonas aeruginosa was investigated, in which SPF Wister rats were infected via trachea with 0.1 ml P. aeruginosa strain PAO579 （ 10^9 CFU/ml） in alginate beads or the planktonic form of this bacterial strain （109 CFU/ml）, and on 3, 7 and 14 d after infection, the bacteriological and pathological changes were observed as well as the expression of the cytokine IL-4 was determined. It was demonstrated that the count of CFU per lung tissue in case of bacteria in alginate beads was significantly higher than that of bacteria in planktonic form, with more severe gross pathologic changes and inflammatory reactions in the alginate bead group in comparison with that of the planktonic forms （ P = 0. 002, P = 0. 004 and P = 0. 002, respectively）. In addition, the expression of IL-4 in the alginate bead group was also higher than that in the planktonic form （P = 0.02, P = 0.02 and P = 0.022, respectively）. A positive correlation between the level of IL-4 expression and the gross lung pathology in alginate bead group existed as demonstrated by simple regression analysis （r = 0.78, P 〈 0.02）. It is concluded that the chronic pulmonary infection with biofilm formation induced by P. aeruginosa tends to have the priority to the Th2 immune response.展开更多
基金National Nature Science Associate Fundation(NSAF) of China (30760084)
文摘Objective： To establish an animal model of P.aeruginosa biofilm associated with chronic pulmonary infection and investigate the pathogenic effects of biofilm. Methods： Experiments in vitro, measuring the MICS, MBCS of levofloxacin（LFX）, ceftazidime（CAZ） in PAO579 in alginate beads and planktonic PAO579. Rats were challenged with 0.1 ml of PAO579（109CFU/ml） in alginate beads or 0.1 ml of planktonic PAO579（109CFU/ml）, 3,7,14 days after challenging, bacteriological, pathological features were observed. Results： The MICS, MBCS of LFX, CAZ in PAO579 in alginate beads were higher than those in planktonic PAO579 in vitro. CFU/lung in alginate beads group was significantly higher than that in planktonic bacteria group（P = 0.002, P = 0.004, P = 0.002, respectively）; macroscopic lung pathology and the inflammation in alginate beads group were significantly more severe compared to those in planktonic bacteria group in vivo. Conclusion： P.aeruginosa biofilm protected bacterium from killing of antibiotics and might mediate the host immune damage in the lung tissue and made bacterium evade the host immune defense.
文摘The expression of IL-4 in a rat model of chronic pulmonary infection biofilm formation induced by Pseudomonas aeruginosa was investigated, in which SPF Wister rats were infected via trachea with 0.1 ml P. aeruginosa strain PAO579 （ 10^9 CFU/ml） in alginate beads or the planktonic form of this bacterial strain （109 CFU/ml）, and on 3, 7 and 14 d after infection, the bacteriological and pathological changes were observed as well as the expression of the cytokine IL-4 was determined. It was demonstrated that the count of CFU per lung tissue in case of bacteria in alginate beads was significantly higher than that of bacteria in planktonic form, with more severe gross pathologic changes and inflammatory reactions in the alginate bead group in comparison with that of the planktonic forms （ P = 0. 002, P = 0. 004 and P = 0. 002, respectively）. In addition, the expression of IL-4 in the alginate bead group was also higher than that in the planktonic form （P = 0.02, P = 0.02 and P = 0.022, respectively）. A positive correlation between the level of IL-4 expression and the gross lung pathology in alginate bead group existed as demonstrated by simple regression analysis （r = 0.78, P 〈 0.02）. It is concluded that the chronic pulmonary infection with biofilm formation induced by P. aeruginosa tends to have the priority to the Th2 immune response.
