Pseudomonas aeruginosa infection in cystic fibrosis: prevent, eradicate or both?

Eber, Ernst; Zach, M

doi:10.1136/thx.2010.138891

Cited by 8 publications

(5 citation statements)

References 45 publications

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“…However, severe lung infections are also connected with deregulated inflammation leading to lung damage, edema, and loss of pulmonary function. [2][3][4][5] IL-17A (often named IL-17) is the best-studied member of the IL-17 cytokine family that comprises at least six IL-17 subtypes (IL-17 A to F). 6 IL-17A contributes to the clearance of microbial infections via the induction of the expression of cytokines, chemokines, and antimicrobial peptides.…”

Section: Introductionmentioning

confidence: 99%

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IL-17A attracts inflammatory cells in murine lung infection with P. aeruginosa

Wonnenberg

Jungnickel²,

Honecker³

et al. 2016

Innate Immun

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IL-17A-dependent immunity is of importance in the protection against extracellular bacterial pathogens. However, IL-17A is also suggested to mediate the pathogenesis of lung diseases, such as acute respiratory distress syndrome. Here, we studied the role of IL-17A in a mouse model of acute pneumonia. IL-17A mediated the expression of keratinocyte-derived chemokine (KC) and the recruitment of inflammatory cells in mice infected with a sub-lethal dose of Pseudomonas aeruginosa. IL-17A deficiency protected mice from lethal P. aeruginosa lung infection. A sub-lethal infection with Streptococcus pneumoniae resulted in increased bacterial burden associated with increased pulmonary inflammation. Thus, the type of infectious bacteria seemed to influence the way in which IL-17A functions during pulmonary infection. Reducing pulmonary inflammation by targeting IL-17A may be a therapeutic option in acute P. aeruginosa pneumonia.

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Section: Introductionmentioning

confidence: 99%

“…However, severe lung infections are also connected with deregulated inflammation leading to lung damage, edema, and loss of pulmonary function. 2–5…”

Section: Introductionmentioning

confidence: 99%

IL-17A attracts inflammatory cells in murine lung infection with P. aeruginosa

Wonnenberg

Jungnickel²,

Honecker³

et al. 2016

Innate Immun

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“…This impairment in ion transport across the epithelium enhances mucus viscosity and interferes with mucociliary clearance, thereby creating an environment susceptible to bacterial infection (4,5). As a result, CF patients have recurrent respiratory bacterial infections, frequently involving Pseudomonas aeruginosa, which is detected in up to 85% of patients (6)(7)(8). Inevitably, persistent bacterial infection in CF patients leads to an influx of neutrophils into the lung that results in a state of chronic inflammation (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

The role for neutrophil extracellular traps in cystic fibrosis autoimmunity

Skopelja¹,

Hamilton²,

Jones³

et al. 2016

JCI Insight

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“…Such mucoidy is due to an overproduction of polysaccharide alginate, which contributes to biofilm formation [ 26 ] and increased resistance to antimicrobials [ 27 ]. It is believed that a non-mucoid phenotype is most often associated with isolates from early infection while mucoid strains are more frequently associated with established infection [ 3 ] and, indeed, poorer patient prognosis [ 28 ]. In our study, the same isolates were identified as proteolytic (associated with damage to tissue [ 29 ]) and siderophore producing (linked to bacterial virulence [ 30 , 31 ]) producing (Table 1 ), although no pattern of changing protease or siderophore activity was discernible.…”

Section: Discussionmentioning

confidence: 99%

A case of failed eradication of cystic fibrosis-related sinus colonisation by Pseudomonas aeruginosa

et al. 2015

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BackgroundPseudomonas aeruginosa is a pathogen associated with cystic fibrosis that has potential to decrease lung function and cause respiratory failure. Paranasal sinuses are increasingly recognised as potential reservoirs for intermittent colonisation by P. aeruginosa. This case documents investigation and outcome of P. aeruginosa recurrence in a male paediatric patient over an eight year period.Case presentationA 12 year old Irish male paediatric cystic fibrosis patient experienced intermittent culturing of P. aeruginosa from the oropharyngeal region, indicating chronic infection of the sinuses despite absence of symptoms, retaining good lung function, and normal bronchoscopy and bronchoalveloar lavage. However, P. aeruginosa was isolated from a sinus wash-out and was identified as a unique strain of P. aeruginosa that was also cultured from cough swabs. Despite treatment, successful eradication from the paranasal sinuses was not achieved.ConclusionsFew reports have addressed the paranasal sinuses as a reservoir for lung infection in cystic fibrosis patients despite increased recognition of the need to investigate this niche. In this case, attempts at eradication of P. aeruginosa present in paranasal sinuses including oral and nebulised antimicrobials proved unsuccessful. However, detection of P. aeruginosa in the paranasal sinuses instigated antimicrobial treatment which may have contributed to prevention of migration to the lower airways. Our outcome provides additional insight and may indicate utility of nasal lavage or nasal endoscopy in paediatric cystic fibrosis patients’ annual review clinic visits.

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Pseudomonas aeruginosa infection in cystic fibrosis: prevent, eradicate or both?

Cited by 8 publications

References 45 publications

IL-17A attracts inflammatory cells in murine lung infection with P. aeruginosa

IL-17A attracts inflammatory cells in murine lung infection with P. aeruginosa

The role for neutrophil extracellular traps in cystic fibrosis autoimmunity

A case of failed eradication of cystic fibrosis-related sinus colonisation by Pseudomonas aeruginosa

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