A Review of the Recent Progress in Treatment of Patients with Diffuse Panbronchiolitis Associated with Pseudomonas aeruginosa Infection in Japan

2015 ◽  
pp. 94-98 ◽  
Author(s):  
Hiroichi Tanimoto
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Recent Progress ◽  
Diffuse Panbronchiolitis ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Role of elastase in a mouse model of chronic respiratory Pseudomonas aeruginosa infection that mimics diffuse panbronchiolitis

2003 ◽  
Vol 52 (6) ◽  
pp. 531-535 ◽  
Author(s):  
Katsunori Yanagihara ◽  
Kazunori Tomono ◽  
Yukihiro Kaneko ◽  
Yoshitsugu Miyazaki ◽  
Kazuhiro Tsukamoto ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Mouse Model ◽  
Histopathological Examination ◽  
Enzymic Activity ◽  
Inflammatory Factor ◽  
Diffuse Panbronchiolitis ◽  
Viable Bacteria ◽  
Respiratory Cells ◽  
Pseudomonas Aeruginosa Infection

Pseudomonas aeruginosa frequently colonizes the respiratory tract of patients suffering from cystic fibrosis (CF) and diffuse panbronchiolitis (DPB). However, the relationship between lung inflammation and extracellular products of P. aeruginosa is not well-defined. To assess the role of elastase released by P. aeruginosa in DPB, a murine model of DPB was employed in this study. Mice were inoculated with either P. aeruginosa PAO1 or PAO-E64; the latter produces elastase with greatly reduced enzymic activity. Throughout the 90-day experiments, counts of viable bacteria from the PAO1- and PAO-E64-infected mice were found to be equivalent. However, the number of lymphocytes isolated from the lungs of PAO-E64-infected mice was significantly lower than the number isolated from the lungs of PAO1-infected animals. Histopathological examination of the lungs of mice infected by PAO1 on day 90 revealed an intense accumulation of chronic respiratory cells surrounding the bronchi, in sharp contrast to the more localized inflammatory response found in those mice infected by PAO-E64. These data suggest that P. aeruginosa elastase (PE) is a potent inflammatory factor in a mouse model of DPB and that the control of PE release by P. aeruginosa may be beneficial for patients with DPB.

The effect of the antiinflammatory IL-1R antagonist anakinra in mice with CF-like lung disease and Pseudomonas aeruginosa infection

Pneumologie ◽  
2016 ◽  
Vol 70 (07) ◽  
Author(s):  
A Schütte ◽  
Z Zhou-Suckow ◽  
J Schatterny ◽  
S Schmidt ◽  
S Hassel ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Lung Disease ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Epidemiology of first/new Pseudomonas aeruginosa infection in cystic fibrosis patients

2010 ◽  
Vol 9 ◽  
pp. S29 ◽  
Author(s):  
L. Zavataro ◽  
G. Taccetti ◽  
L. Cariani ◽  
N. Ravenni ◽  
G. Braccini ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Pseudomonas Aeruginosa Infection

scholarly journals Rapid evolution and host immunity drive the rise and fall of carbapenem resistance during an acute Pseudomonas aeruginosa infection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Rachel Wheatley ◽  
Julio Diaz Caballero ◽  
Natalia Kapel ◽  
Fien H. R. de Winter ◽  
Pramod Jangir ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Efflux Pump ◽  
Rapid Evolution ◽  
Carbapenem Resistance ◽  
Host Immunity ◽  
High Definition ◽  
Loss Of Resistance ◽  
Pseudomonas Aeruginosa Infection ◽  
Second Wave

AbstractIt is well established that antibiotic treatment selects for resistance, but the dynamics of this process during infections are poorly understood. Here we map the responses of Pseudomonas aeruginosa to treatment in high definition during a lung infection of a single ICU patient. Host immunity and antibiotic therapy with meropenem suppressed P. aeruginosa, but a second wave of infection emerged due to the growth of oprD and wbpM meropenem resistant mutants that evolved in situ. Selection then led to a loss of resistance by decreasing the prevalence of low fitness oprD mutants, increasing the frequency of high fitness mutants lacking the MexAB-OprM efflux pump, and decreasing the copy number of a multidrug resistance plasmid. Ultimately, host immunity suppressed wbpM mutants with high meropenem resistance and fitness. Our study highlights how natural selection and host immunity interact to drive both the rapid rise, and fall, of resistance during infection.

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