Pathogenesis and clinical manifestations of chronic colonization by Pseudomonas aeruginosa and its biofilms in the airway tract

Kobayashi, Hiroyoshi; Kobayashi, Osamu; Kawai, Shinya

doi:10.1007/s10156-008-0691-3

Cited by 32 publications

(37 citation statements)

References 244 publications

(233 reference statements)

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“…The mucoid phenotype is associated with a change in morphology from flagellar motility to twitching motility, a loss of pili and flagella, and exopolysaccharide alginate production by guanosine diphospho-D-mannose dehydrogenase (GMD). Within mature (145). Immune complex deposition in the airway, with resultant neutrophil chemotaxis, leads to lung damage (95).…”

Section: Inhibition Of Biofilmsmentioning

confidence: 99%

“…Macrolides decreased the number of viable bacteria in a murine model of biofilm-associated respiratory P. aeruginosa infection (335). Decreased biofilm formation may be due to inhibition of the GMD production cycle (145,188) or to prevention of pilus-dependent twitching motility (328). Long-term treatment with clarithromycin can decrease serum immune complexes in patients with DPB (144).…”

Section: Inhibition Of Biofilmsmentioning

confidence: 99%

“…Long-term treatment with clarithromycin can decrease serum immune complexes in patients with DPB (144). Because macrolides can disrupt biofilms and revert bacterial morphology to a planktonic state, combining macrolides with antipseudomonal antibiotics may be more effective than using antibiotics alone for bacterial killing (145).…”

Section: Inhibition Of Biofilmsmentioning

confidence: 99%

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Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

2010

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SUMMARY Macrolides have diverse biological activities and an ability to modulate inflammation and immunity in eukaryotes without affecting homeostatic immunity. These properties have led to their long-term use in treating neutrophil-dominated inflammation in diffuse panbronchiolitis, bronchiectasis, rhinosinusitis, and cystic fibrosis. These immunomodulatory activities appear to be polymodal, but evidence suggests that many of these effects are due to inhibition of extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation and nuclear factor kappa B (NF-κB) activation. Macrolides accumulate within cells, suggesting that they may associate with receptors or carriers responsible for the regulation of cell cycle and immunity. A concern is that long-term use of macrolides increases the emergence of antimicrobial resistance. Nonantimicrobial macrolides are now in development as potential immunomodulatory therapies.

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Section: Inhibition Of Biofilmsmentioning

confidence: 99%

Section: Inhibition Of Biofilmsmentioning

confidence: 99%

Section: Inhibition Of Biofilmsmentioning

confidence: 99%

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Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

2010

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“…It is extremely robust and capable of surviving in challenging and varied environmental niches, as exemplified by its isolation from jet plane fuel and bottles of disinfectant fluid [1]. This adaptability is conferred by its large genome (approximately 6 Mb) and ability to survive as either a planktonic organism or as a member of a codependent bacterial community within the confines of a ''biofilm'' [2,3].…”

Section: Introductionmentioning

confidence: 99%

Targeting iron uptake to controlPseudomonas aeruginosainfections in cystic fibrosis

et al. 2012

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The aerobic Gram-negative bacterium Pseudomonas aeruginosa is an opportunistic pathogen responsible for life-threatening acute and chronic infections in humans. As part of chronic infection P. aeruginosa forms biofilms, which shield the encased bacteria from host immune clearance and provide an impermeable and protective barrier against currently available antimicrobial agents.P. aeruginosa has an absolute requirement for iron for infection success. By influencing cell-cell communication (quorum sensing) and virulence factor expression, iron is a powerful regulator of P. aeruginosa behaviour. Consequently, the imposed perturbation of iron acquisition systems has been proposed as a novel therapeutic approach to the treatment of P. aeruginosa biofilm infection.In this review, we explore the influence of iron availability on P. aeruginosa infection in the lungs of the people with the autosomal recessive condition cystic fibrosis as an archetypal model of chronic P. aeruginosa biofilm infection. Novel therapeutics aimed at disrupting P. aeruginosa are discussed, with an emphasis placed on identifying the barriers that need to be overcome in order to translate these promising in vitro agents into effective therapies in human pulmonary infections. @ERSpublications Can targeting iron uptake be utilised to control Pseudomonas aeruginosa infections in cystic fibrosis patients?

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“…aeruginosa is a versatile, aerobic gram-negative bacterium which is widespread in the terrestrial environment. It is an extremely robust organism and, as exemplified by its isolation from jet plane fuel and bottles of disinfectant fluid, capable of surviving in challenging and varied environmental niches (88). This adaptability is conferred by both its very large genome (~6000 genes, ~500 of which are involved in regulatory processes) and its ability to survive as either a planktonic organism, or as a member of co-dependent bacterial communities within the confines of a "biofilm" (89,90).…”

Section: Pseudomonas Aeruginosamentioning

confidence: 99%

Investigating the host and bacterial factors in cystic fibrosis that promote persistence of infection in the lung

Smith¹

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Pathogenesis and clinical manifestations of chronic colonization by Pseudomonas aeruginosa and its biofilms in the airway tract

Cited by 32 publications

References 244 publications

Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

Mechanisms of Action and Clinical Application of Macrolides as Immunomodulatory Medications

Targeting iron uptake to controlPseudomonas aeruginosainfections in cystic fibrosis

Investigating the host and bacterial factors in cystic fibrosis that promote persistence of infection in the lung

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