Pseudomonas aeruginosa -Catecholamine Inotrope Interactions

Freestone, Primrose; Hirst, Robert A.; Sandrini, Sara M.; Sharaff, Fathima; Fry, Helen; Hyman, Stefan C.; O’Callaghan, Chris

doi:10.1378/chest.11-2614

Cited by 90 publications

(70 citation statements)

References 40 publications

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“…The luminal surfaces of the lungs are significantly different from those of the GI tract and ecological principles are the driving force of lung microbiome-immmune system interactions (“immunoecology”). Numerous byproducts of the host inflammatory response are known growth factors for select bacterial species, including catecholamines, 68 inflammatory cytokines, 69–71 increased temperature, 72,73 and free ATP. 72,73 The extracellular nutrient supply for bacteria in the airways, which is severely limited during health, is abruptly increased by the presence of mucus and vascular permeability.…”

Section: Discussionmentioning

confidence: 99%

The respiratory tract microbiome and lung inflammation: a two-way street

2017

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The lungs are not sterile or free from bacteria; rather, they harbor a distinct microbiome whose composition is driven by different ecological rules than for the gastrointestinal tract. During disease, there is often a shift in community composition towards Gammaproteobacteria, the bacterial class that contains many common lung-associated gram-negative “pathogens.” Numerous byproducts of host inflammation are growth factors for these bacteria. The extracellular nutrient supply for bacteria in the lungs, which is severely limited during health, markedly increases due to the presence of mucus and vascular permeability. While Gammaproteobacteria benefit from airway inflammation, they also encode molecular components that promote inflammation, potentially creating a cyclical inflammatory mechanism. In contrast, Prevotella species that are routinely acquired via microaspiration from the oral cavity may participate in immunologic homeostasis of the airways. v Areas of future research include determining for specific lung diseases (1) whether an altered lung microbiome initiates disease pathogenesis, promotes chronic inflammation, or is merely a marker of injury and inflammation, (2) whether the lung microbiome can be manipulated therapeutically to change disease progression, (3) what molecules (metabolites) generated during an inflammatory response promote cross-kingdom signaling, and (4) how the lung “ecosystem” collapses during pneumonia, to be dominated by a single pathogen.

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Section: Discussionmentioning

confidence: 99%

The respiratory tract microbiome and lung inflammation: a two-way street

2017

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“…Increased cough accelerates microbial efflux, and the numbers and activation of inflammatory cells increase 60 . Byproducts of the host inflammatory response such as inflammatory cytokines 61-63 , catecholamines 64 , increased temperature 53, 65 , glucose and free ATP 65 are known growth factors for select bacterial species, creating selectively favorable growth conditions. Bronchoconstriction alters regional oxygen concentration and pH.…”

Section: The Microbial Ecology and Topography Of The Human Respiratormentioning

confidence: 99%

“…A rich recent literature has demonstrated that the behavior of a given bacterial strain (as assessed either by gene expression or in vitro or in vivo virulence and immunogenicity) is strongly influenced by the same environmental factors that differentially alter bacterial growth rates: temperature 53, 65 , concentration of host-derived cytokines and catecholamines 63, 64 and presence of free glucose 65 . Further, the behavior and virulence of a single strain is dramatically influenced by the composition of the bacterial community sharing its ecologic niche 123 , mediated by direct and indirect microbe-microbe interactions 124, 125 .…”

Section: Key Lessons and Directions For Studymentioning

confidence: 99%

The role of the microbiome in exacerbations of chronic lung diseases

2014

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Summary Culture-independent microbiological techniques have revealed a previously unappreciated complexity to the bacterial microbiome of the respiratory tract, forcing reconsideration of the interactions between host, bacteria and the pathogenesis of exacerbations of chronic lung disease. The composition of the lung microbiome is determined by microbial immigration, elimination, and the relative growth rates of its members; all of these change dramatically in chronic lung disease and further during exacerbations. Exacerbations lack key features of bacterial infections, including increased bacterial burden and decreased community diversity. We propose instead that exacerbations are occasions of respiratory dysbiosis: a disordered respiratory microbial ecosystem with negative effects on host biology. Respiratory dysbiosis provokes a dysregulated host immune response, which in turn alters microbial growth conditions in patient airways, further promoting dysbiosis and perpetuating a coupled cycle of inflammation and disordered microbiota. Differences in baseline respiratory microbiota may help explain the “frequent-exacerbator” phenotype observed across multiple disease states, and may provide novel targets for therapeutic intervention.

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“…Thompson et al (1999) demonstrated that in dopamine-medicated cardiac surgery patients, plasma NE levels rose to as high as 9.24 mM. Work from Freestone et al (2012) found that levels of NE and dopamine in this range and lower (5 mM) markedly increased Pseudomonas aeruginosa growth, biofilm formation and attachment to human ciliated epithelia. A later work by Sandrini et al (2014) demonstrated that 5 mM dopamine and NE were stimulatory to the growth of S. pneumoniae, enhancing biofilm formation and expression of genes involved in metabolism and virulence.…”

Section: Catecholamine Levels In Vivomentioning

confidence: 99%

“…A later work by Sandrini et al (2014) demonstrated that 5 mM dopamine and NE were stimulatory to the growth of S. pneumoniae, enhancing biofilm formation and expression of genes involved in metabolism and virulence. Interestingly, acutely ill ventilated patients are at significant risk of developing ventilator-associated pneumonia from bacteria such as P. aeruginosa and S. pneumoniae (Freestone et al 2012), and catecholamine solutions are occasionally directly administered to the airway to reduce inflammation (Stannard & O'Callaghan 2002).…”

Section: Catecholamine Levels In Vivomentioning

confidence: 99%

Microbial endocrinology: host–bacteria communication within the gut microbiome

Sandrini¹,

Aldriwesh²,

Alruways³

et al. 2015

Journal of Endocrinology

113

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The human body is home to trillions of micro-organisms, which are increasingly being shown to have significant effects on a variety of disease states. Evidence exists that a bidirectional communication is taking place between us and our microbiome co-habitants, and that this dialogue is capable of influencing our health in a variety of ways. This review considers how host hormonal signals shape the microbiome, and what in return the microbiome residents may be signalling to their hosts.

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Pseudomonas aeruginosa -Catecholamine Inotrope Interactions

Cited by 90 publications

References 40 publications

The respiratory tract microbiome and lung inflammation: a two-way street

The respiratory tract microbiome and lung inflammation: a two-way street

The role of the microbiome in exacerbations of chronic lung diseases

Microbial endocrinology: host–bacteria communication within the gut microbiome

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