Polyamines in Cystic Fibrosis

McEVOY, Finbar A.; Hartley, Claire

doi:10.1203/00006450-197509000-00007

Cited by 22 publications

(10 citation statements)

References 7 publications

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“…Polyamines have been reported to be in the mid-to-high micromolar range in the human intestinal lumen, which is below the concentration shown in this study to inhibit autoagglutination [48], [49]. This observation is consistent with the fact that V. cholerae can easily colonize most individuals if ingested in sufficient amounts.…”

Section: Discussionsupporting

confidence: 89%

Effects of Polyamines on Vibrio cholerae Virulence Properties

2013

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Vibrio cholerae is the causative agent of the severe enteric disease cholera. To cause cholera the bacterium must be able to synthesize both cholera toxin (CT) and toxin-coregulated pilus (TCP) which mediates autoagglutination and is required for colonization of the small intestine. Only a few environmental signals have been shown to regulate V. cholerae virulence gene expression. Polyamines, which are ubiquitous in nature, and have been implicated in regulating virulence gene expression in other bacteria, have not been extensively studied for their effect on V. cholerae virulence properties. The objective of this study was to test the effect of several polyamines that are abundant in the human intestine on V. cholerae virulence properties. All of the polyamines tested inhibited autoagglutination of V. cholerae O1 classical strain in a concentration dependent manner. Putrescine and cadaverine decreased the synthesis of the major pilin subunit, TcpA, spermidine increased its production, and spermine had no effect. Putrescine and spermidine led to a decrease and increase, respectively, on the relative abundance of TCP found on the cell surface. Spermine led to a small reduction in cholera toxin synthesis whereas none of the other polyamines had an effect. The polyamines did not affect pili bundling morphology, but caused a small reduction in CTXφ transduction, indicating that the TCP present on the cell surface may not be fully functional. We hypothesize the inhibition of autoagglutination is likely to be caused by the positively charged amine groups on the polyamines electrostatically disrupting the pili-pili interactions which mediate autoagglutination. Our results implicate that polyamines may have a protective function against colonization of the small intestine by V. cholerae.

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Section: Discussionsupporting

confidence: 89%

Effects of Polyamines on Vibrio cholerae Virulence Properties

2013

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“…In the jejunum of adult rats, the spermidine concentration is about 0.1 m m and the spermine concentration is about 0.5 m m (Hinuma et al 1992). In young humans, the duodenal fluid contains about 95 μ m spermidine and 46 μ m spermine (McEvoy & Hartley, 1975). In adult humans, the jejunum concentration is about 86 μ m for putrescine, 25 μ m for spermidine and 3.75 μ m for spermine (Benamouzig et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Intestinal effects of long‐lasting spermine ingestion by suckling rats

Deloyer

Peulen

Dandrifosse

2005

Experimental Physiology

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Spermine ingestion induces the precocious maturation of the small intestine in suckling rats. Previous observations suggest that spermine-induced intestinal maturation is a two-step phenomenon. The first step is the elimination of immature enterocytes (4-10 h post spermine ingestion) and the second step is the replacement of previous immature cells by adult-type enterocytes (2-3 days post initial spermine administration). The spermine-induced maturation is reversible when spermine administration is stopped. This work was undertaken in order to check whether the extension of polyamine administration (for 3-7 days) after the appearance of spermine-induced maturation can retain the mature state of the small intestine. Our results indicate that extension of spermine administration does not prevent some parameters (sucrase and maltase specific activities) reverting to a typical 'immature' value while others remain at a typical 'mature' level (mucosal weight and lactase specific activity). Our results show that there are at least two different mechanisms in required for the control of spermine-induced maturation of the small intestine.

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“…For example, under the same experimental conditions as employed in the present work, 2 mmol/l glycochenodeoxycholate, a common human bile salt, totally prevented the formation of HAP for at least 4 days (13); in comparison, 2 mmol/l spermine, the most effective polyamine, had only a slight effect. The concentration of bile salts in bile greatly exceeds the concentration of polyamines ( < 2 mmol/l) (18), which suggests that polyamines are likely to have only a minor role in inhibiting HAP formation in vivo. Further, it would seem to be unwise to attempt to increase biliary polyamine concentrations in an attempt to increase their potency because polyamines can promote the nucleation of cholesterol from native human bile (19).…”

Section: Discussionmentioning

confidence: 99%

“…In most extracellular fluids the concentration of polyamines is very low (-1 pmol/1), but the proximal gut of the rat contains high levels of putrescine (2-3 mmol/l) and cadaverine (-1 mmol/1) that are synthesized by the colonic microflora and transported to the duodenum by the enterohepatic circulation (1 7). Relatively high concentrations of spermine and spermidine have been measured in human bile, and it was suggested that the biliary route is a significant pathway for polyamine excretion (18). Polyamines have been proposed as potential nucleating factors in bile, based on their ability to promote cholesterol precipitation (19).…”

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confidence: 99%

Inhibition of calcium hydroxyapatite formation by polyamines

Crowther

Pritchard

Qiu

et al. 1993

Liver

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ABSTRACT— The lithogenic potential of bile depends not only on supersaturation of solutes but also on the presence of pro‐ and anti‐nucleating factors. For example, glycine‐conjugated dihydroxy bile salt dimers are potent inhibitors of calcium hydroxyapatite precipitation that function by “poisoning” the nascent crystal. Although most inhibitors of apatite formation are anions, theoretically polycations should also be effective, and because significant concentrations of polyamines are present in bile, we have investigated the ability of these molecules to inhibit apatite formation. In vitro, each polyamine (2–10 mmol/l) was able to inhibit apatite formation, and the inhibiting power was correlated with ionic charge. Thus putrescine (2+) was the weakest inhibitor and spermine (4+) was the strongest. Mixtures of polyamines were less effective than were the individual polyamines, except at higher concentrations. Although polyamines were effective over short periods of time (270 min), over longer times (3 days) spermine was unable to prevent apatite formation. Using infrared spectroscopy, we found no evidence for interaction between phosphate ions and spermine in solution. Taken together, these results suggest that polyamines are modest inhibitors of apatite formation that likely function by retarding the dissolution of the intermediate amorphous calcium phosphate phase.

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Polyamines in Cystic Fibrosis

Cited by 22 publications

References 7 publications

Effects of Polyamines on Vibrio cholerae Virulence Properties

Effects of Polyamines on Vibrio cholerae Virulence Properties

Intestinal effects of long‐lasting spermine ingestion by suckling rats

Inhibition of calcium hydroxyapatite formation by polyamines

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