The Virulence of Pseudomonas aeruginosa

Pollack, Matthew

doi:10.1093/clinids/6.supplement_3.s617

Cited by 103 publications

(71 citation statements)

References 62 publications

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“…Pseudomonal infection is very different in the setting of CF versus non-CF in terms of disease process and resolution. In contrast to pseudomonal chronic infections similar to or typically seen in CF, an invasive Pa infection involves bacterial attachment, colonization, local infection, and bloodstream dissemination or systemic disease (Pollack, 2000). Pseudomonal colonization and adherence to the host airway mucosal surface without entering the blood stream is most evident in the setting of CF (Valderrey et al, 2010).…”

Section: Clinical Characteristics Of Pseudomonal Infection In the Airmentioning

confidence: 99%

Chronic pulmonary pseudomonal infection in patients with cystic fibrosis: A model for early phase symbiotic evolution

Qin

2014

Critical Reviews in Microbiology

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To cite this article: Xuan Qin (2016) Chronic pulmonary pseudomonal infection in patients with cystic fibrosis: A model for early phase symbiotic evolution, Critical Reviews in Microbiology, 42:1, 144-157, DOI: 10.3109/1040841X.2014 AbstractGain of ''antimicrobial resistance'' and ''adaptive virulence'' has been the dominant view of Pseudomonas aeruginosa (Pa) in cystic fibrosis (CF) in the progressively damaged host airway over the course of this chronic infection. However, the pathogenic effects of CF airway-adapted Pa strains are notably reduced. We propose that CF Pa and other bacterial cohabitants undergo host adaptation which resembles the changes found in bacterial symbionts in animal hosts. Development of clonally selected and intraspecific isogenic Pa strains which display divergent colony morphology, growth rate, auxotrophy, and antibiotic susceptibility in vitro suggests an adaptive sequence of infective exploitation-parasitism-symbiotic evolution driven by host defenses. Most importantly, the emergence of CF pseudomonal auxotrophy is frequently associated with a few specific amino acids. The selective retention or loss of specific amino acid biosynthesis in CF-adapted Pa reflects bacterium-host symbiosis and coevolution during chronic infection, not nutrient availability. This principle also argues against the long-standing concept of dietary availability leading to evolution of essential amino acid requirements in humans. A novel model of pseudomonal adaptation through multicellular bacterial syntrophy is proposed to explain early events in bacterial gene decay and decreased (not increased) virulence due to symbiotic response to host defense.

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Section: Clinical Characteristics Of Pseudomonal Infection In the Airmentioning

confidence: 99%

Chronic pulmonary pseudomonal infection in patients with cystic fibrosis: A model for early phase symbiotic evolution

Qin

2014

Critical Reviews in Microbiology

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“…aeruginosa can produce a number of cell-associated and extracellular virulence factors which contribute to its pathogenesis (Doring et al, 1984(Doring et al, , 1985(Doring et al, , 1987Jaeger, 1994 ;Van Delden & Iglewski, 1998). The extracellular virulence factors include proteases (elastase, Staphylolytic protease and alkaline protease), pigments (pyocyanin, pyoverdine), haemolysins, exoenzyme S and exotoxin A (Pollack, 1984 ;Van Delden & Iglewski, 1998). In P. aeruginosa, it has been demonstrated that the production of most of the extracellular virulence factors is controlled by quorum sensing systems in vitro Van Delden & Iglewski, 1998).…”

Section: Introductionmentioning

confidence: 99%

Pseudomonas aeruginosa mutations in lasI and rhlI quorum sensing systems result in milder chronic lung infection

et al. 2001

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To understand the importance of quorum sensing in chronic Pseudomonas aeruginosa lung infection, the in vivo pathogenic effects of the wild-type P. aeruginosa PAO1 and its double mutant, PAO1 lasI rhlI, in which the signalgenerating parts of the quorum sensing systems are defective were compared. The rat model of P. aeruginosa lung infection was used in the present study. The rats were killed on days 3, 7, 14 and 28 after infection with the P. aeruginosa strains. The results showed that during the early stages of infection, the PAO1 double mutant induced a stronger serum antibody response, higher production of pulmonary interferon γ, and more powerful blood polymorphonuclear leukocyte (PMN) chemiluminescence compared to its wild-type counterpart. On days 14 and 28 post-infection, significantly milder lung pathology, a reduction in the number of mast cells present in the lung foci, a reduced number of lung bacteria, and minor serum IgG and IgG1 responses but increased lung interferon γ production were detected in the group infected with the PAO1 double mutant when compared with the PAO1-infected group. Delayed immune responses were observed in the PAO1-infected group and they might be associated with the production of virulence factors that are controlled by the quorum sensing systems. The conclusion of this study is that functional lasI and rhlI genes of P. aeruginosa PAO1 play a significant role during lung infection.

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“…Production of by AM in response to PNR may also operate within the cytokine network between AM and other neighboring non-immune respiratory cells. These data suggest the contribution of PNR to neutrophil accumulation in bronchopulmonary infections due to P. aeruginosa, frequently associated with ARDS in immunocompromised or mechanically ventilated patients (20,29).…”

Section: Induction Of Il-8 By A549 Cellsmentioning

confidence: 64%

“…Interleukin (20). Nosocomial pneumonia caused by P. aeruginosa is associated with a high mortality, despite recent advances in antimicrobial chemotherapy (2,19).…”

Section: Introductionmentioning

confidence: 99%

Induction of Interleukin 8 (IL‐8) Production by Pseudomonas Nitrite Reductase in Human Alveolar Macrophages and Epithelial Cells

Sar

Oishi

Matsushima

et al. 1999

Microbiology and Immunology

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The Virulence of Pseudomonas aeruginosa

Cited by 103 publications

References 62 publications

Chronic pulmonary pseudomonal infection in patients with cystic fibrosis: A model for early phase symbiotic evolution

Chronic pulmonary pseudomonal infection in patients with cystic fibrosis: A model for early phase symbiotic evolution

Pseudomonas aeruginosa mutations in lasI and rhlI quorum sensing systems result in milder chronic lung infection

Induction of Interleukin 8 (IL‐8) Production by Pseudomonas Nitrite Reductase in Human Alveolar Macrophages and Epithelial Cells

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