Gut-Derived Sepsis Occurs When the Right Pathogen With the Right Virulence Genes Meets the Right Host

Alverdy, John C.; Holbrook, Christopher; Rocha, Flavio; Seiden, Louis; Licheng, Richard; Wu, Kan; Musch, Mark W.; Chang, Eugene B.; Ohman, Dennis E.; Suh, Sanj

doi:10.1097/00000658-200010000-00003

Cited by 191 publications

(154 citation statements)

References 30 publications

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“…Increased direct release of catecholamines by the enteric nervous system (ENS) under stress has also been demonstrated experimentally by Zhou et al who showed that in the GI tract of rats expression of tyrosine hydroxylase (the rate limiting enzyme of catecholamine biosynthesis; see Figure 1) became up-regulated in response to physical stress such as surgical perforation of the bowel (Zhou et al, 2004). A related study by Alverdy et al employed a mouse model of surgical stress (a partial hepatectomy v. a sham laparotomy) to show that surgery can cause direct increases in the levels of NA released into the GI tract (Alverdy et al, 2000). Alverdy and colleagues also reported that mice subjected to the partial hepatectomy became significantly more susceptible to gut-derived sepsis by the opportunistic pathogen Pseudomonas aeruginosa, possibly because of NA-induced increases in the expression of the PA-I lectin, an essential P. aeruginosa host attachment factor (Alverdy et al, 2000).…”

Section: Microbial Endocrinologymentioning

confidence: 99%

“…A related study by Alverdy et al employed a mouse model of surgical stress (a partial hepatectomy v. a sham laparotomy) to show that surgery can cause direct increases in the levels of NA released into the GI tract (Alverdy et al, 2000). Alverdy and colleagues also reported that mice subjected to the partial hepatectomy became significantly more susceptible to gut-derived sepsis by the opportunistic pathogen Pseudomonas aeruginosa, possibly because of NA-induced increases in the expression of the PA-I lectin, an essential P. aeruginosa host attachment factor (Alverdy et al, 2000).…”

Section: Microbial Endocrinologymentioning

confidence: 99%

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Stress and microbial endocrinology: prospects for ruminant nutrition

Freestone

Lyte

2010

Animal

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The feed efficiency of ruminant meat and dairy livestock can be significantly influenced by factors within their living environments. In particular, events perceived by the animals as stressful (such as parturition, transport or handling) have been found to affect susceptibility to infection. It has been well documented that even minor stress such as weighing can result in an increase in colonisation and faecal shedding of enteric pathogens such as Salmonella enterica and Escherichia coli O157:H7. Such infections affect both ruminant overall health and therefore performance, and are a particular problem for the meat production industries. Prior explanations for stress enhancing the likelihood of infection is that activation of the sympathetic nervous system under stress leads to the release of neuroendocrine mediators such as the catecholamine stress hormones noradrenaline and adrenaline, which may impair innate and adaptive immunity. More recently, however, another equally compelling explanation, viewed through the lens of the newly recognised microbiological discipline of microbial endocrinology is that the myriad of bacteria within the ruminant digestive tract are as responsive to the hormonal output of stress as the cells of their host. Work from our laboratories has shown that enteric pathogens have evolved systems for directly sensing stress hormones. We have demonstrated that even brief exposure of enteric pathogens to physiological concentrations of stress hormones can result in massive increases in growth and marked changes in expression of virulence factors such as adhesins and toxins. Happy, less stressed ruminants may therefore be better-nourished animals and safer sources of meat. This article reviews evidence that stress, as well as affecting nutrition, in ruminants is correlated with increased risk of enteric bacterial infections, and examines the molecular mechanisms that may be at work in both processes.

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Section: Microbial Endocrinologymentioning

confidence: 99%

Section: Microbial Endocrinologymentioning

confidence: 99%

Stress and microbial endocrinology: prospects for ruminant nutrition

Freestone

Lyte

2010

Animal

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“…Furthermore, although P. aeruginosa is better known as a respiratory pathogen rather than an intestinal pathogen, this strain is one of the most common opportunistic pathogens in the normal gastrointestinal tract (Alverdy et al, 2000), and in critically-ill and immunocompromised Resistance to antivirulence compounds T Maeda et al patients where stress levels are high, Pseudomonas sp. counts have been shown to increase by as much as 100-fold (Shimizu et al, 2006) leading to the expression of virulence determinants (Alverdy et al, 2000) that are controlled by QS (Hegde et al, 2009) (just the presence of P. aeruginosa in the gastrointestinal tract of critically-ill surgical patients has been associated with nearly 70% mortality (Alverdy et al, 2000)). Hence, growth on this carbon source is physiologically relevant and P. aeruginosa infections in the gastrointestinal tract are pertinent.…”

Section: Introductionmentioning

confidence: 99%

Quorum quenching quandary: resistance to antivirulence compounds

et al. 2011

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Quorum sensing (QS) is the regulation of gene expression in response to the concentration of small signal molecules, and its inactivation has been suggested to have great potential to attenuate microbial virulence. It is assumed that unlike antimicrobials, inhibition of QS should cause less Darwinian selection pressure for bacterial resistance. Using the opportunistic pathogen Pseudomonas aeruginosa, we demonstrate here that bacterial resistance arises rapidly to the best-characterized compound that inhibits QS (brominated furanone C-30) due to mutations that increase the efflux of C-30. Critically, the C-30-resistant mutant mexR was more pathogenic to Caenorhabditis elegans in the presence of C-30, and the same mutation arises in bacteria responsible for chronic cystic fibrosis infections. Therefore, bacteria may evolve resistance to many new pharmaceuticals thought impervious to resistance.

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“…The opportunistic pathogen Pseudomonas aeruginosa synthesizes two lectins, LecA and LecB (also known as PA-IL and PA-IIL), with specificity for galactose and fucose, respectively. Many roles have been suggested for these lectins, including adhesion of the bacterium to airway epithelial cells and injury to cells (1,15). Furthermore, LecB was recently reported to be involved in biofilm formation (27).…”

mentioning

confidence: 99%

Pseudomonas aeruginosa LecB Is Involved in Pilus Biogenesis and Protease IV Activity but Not in Adhesion to Respiratory Mucins

2006

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Pseudomonas aeruginosa expresses two lectins which are implicated in adhesion and biofilm formation. In this study, we demonstrate that P. aeruginosa LecB is involved in pilus biogenesis and proteolytic activity. Moreover, neither lectin was involved in adhesion to human tracheobronchial mucin. We infer that some of the ascribed functions are secondary effects on other systems rather than effects of the lectins themselves.

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Gut-Derived Sepsis Occurs When the Right Pathogen With the Right Virulence Genes Meets the Right Host

Cited by 191 publications

References 30 publications

Stress and microbial endocrinology: prospects for ruminant nutrition

Stress and microbial endocrinology: prospects for ruminant nutrition

Quorum quenching quandary: resistance to antivirulence compounds

Pseudomonas aeruginosa LecB Is Involved in Pilus Biogenesis and Protease IV Activity but Not in Adhesion to Respiratory Mucins

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