Polyamines in Gut Inflammation and Allergy

Peulen, Olivier; Deloyer, Patricia; Devillé, Christelle; Dandrifosse, Guy

doi:10.2174/1568014043483599

Cited by 10 publications

(7 citation statements)

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“…In this context, polyamine levels could be regarded as markers of a hyperproliferative state in response to toxic effects of gliadin. This behavior by polyamines has already been reported during inflammation of intestine leading to derangement of the mucosa [ 34 ].…”

Section: Discussionsupporting

confidence: 67%

Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines

et al. 2014

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BackgroundCeliac disease is characterized by enhanced intestinal paracellular permeability due to alterations of function and expression of tight junction (TJ) proteins including ZO-1, Claudin-1 and Occludin. Polyamines are pivotal in the control of intestinal barrier function and are also involved in the regulation of intercellular junction proteins. Different probiotic strains may inhibit gliadin-induced toxic effects and the Lactobacillus rhamnosus GG (L.GG) is effective in the prevention and treatment of gastrointestinal diseases. Aims of the study were to establish in epithelial Caco-2 cells whether i) gliadin affects paracellular permeability and polyamine profile; ii) co-administration of viable L.GG, heat-killed L.GG (L.GG-HK) or its conditioned medium (L.GG-CM) preserves the intestinal epithelial barrier integrity. Additionally, the effects of L.GG on TJ protein expression were tested in presence or absence of polyamines.ResultsAdministration of gliadin (1 mg/ml) to Caco-2 cells for 6 h caused a significant alteration of paracellular permeability as demonstrated by the rapid decrease in transepithelial resistance with a concomitant zonulin release. These events were followed by a significant increase in lactulose paracellular transport and a slight lowering in ZO-1 and Occludin expression without affecting Claudin-1. Besides, the single and total polyamine content increased significantly. The co-administration of viable L.GG (108 CFU/ml), L.GG-HK and L.GG-CM with gliadin significantly restored barrier function as demonstrated by transepithelial resistance, lactulose flux and zonulin release. Viable L.GG and L.GG-HK, but not L.GG-CM, led to a significant reduction in the single and total polyamine levels. Additionally, only the co-administration of viable L.GG with gliadin significantly increased ZO-1, Claudin-1 and Occludin gene expression compared to control cells. When Caco-2 cells treated with viable L.GG and gliadin were deprived in the polyamine content by α-Difluoromethylornithine, the expression of TJ protein mRNAs was not significantly different from that in controls or cells treated with gliadin alone.ConclusionsGliadin modifies the intestinal paracellular permeability and significantly increases the polyamine content in Caco-2 cells. Concomitant administration of L.GG is able to counteract these effects. Interestingly, the presence of cellular polyamines is necessary for this probiotic to exert its capability in restoring paracellular permeability by affecting the expression of different TJ proteins.

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Section: Discussionsupporting

confidence: 67%

Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines

et al. 2014

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“…Polyamines are important mediators of inflammation [3], and studies have indicated that polyamine biosynthesis is increased during sepsis [4, 5]. Although the functions of the up-regulated polyamines during sepsis and inflammation are not clear, we hypothesize that polyamine levels may increase during inflammation to help fuel hypusine biosynthesis, which is a polyamine-dependent reaction.…”

mentioning

confidence: 91%

Eukaryotic Translation Initiation Factor 5A Small Interference RNA–Liposome Complexes Reduce Inflammation and Increase Survival in Murine Models of Severe Sepsis and Acute Lung Injury

et al. 2008

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Background Many novel therapeutics have failed to reduce all-cause mortality associated with severe sepsis. Eukaryotic translation initiation factor 5A (eIF5A) is a regulator of apoptosis as well as inflammatory cell activation, making it a potential target for sepsis therapy. Methods In a murine model of severe sepsis, mice were intraperitoneally challenged with lipopolysaccharide (LPS). Mice were treated both before and after LPS challenge with liposome complexes containing either an eIF5A-specific or control small interference RNA (siRNA), and both survival and serum concentrations of inflammatory cytokines were monitored. The ability of eIF5A siRNA to reduce inflammatory cytokines was also tested in a model of acute lung injury established by intranasal administration of LPS to mice. Results There was a statistically significant increase in the rate of survival for mice intraperitoneally challenged with LPS that received eIF5A siRNA, compared with that noted for mice that received control siRNA (71% vs. 5%; P < .001), as well as a reduction in cytokine expression in serum. Concentrations of proinflammatory cytokines were also reduced in the lung homogenates and serum of mice that were intranasally challenged with LPS and received eIF5A siRNA (P ≤ .05). Conclusions eIF5A siRNA-liposome complexes reduced inflammation and contributed to increased survival in a model of severe sepsis, decreased inflammation in a model of acute lung injury, and should be considered for clinical use.

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“…6), is considered to be essential for proliferation and differentiation of the renewing intestinal mucosa [37]. In several studies, the authors suggested that polyamine deficiency can be the cause of inflammation [38, 39].…”

Section: Discussionmentioning

confidence: 99%

A novel graph theoretical approach for modeling microbiomes and inferring microbial ecological relationships

et al. 2019

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BackgroundMicrobiomes play vital roles in shaping environments and stabilize them based on their compositions and inter-species relationships among its species. Variations in microbial properties have been reported to have significant impact on their host environment. For example, variants in gut microbiomes have been reported to be associated with several chronic conditions, such as inflammatory disease and irritable bowel syndrome. However, how microbial bacteria contribute to pathogenesis still remains unclear and major research questions in this domain remain unanswered.MethodsWe propose a split graph model to represent the composition and interactions of a given microbiome. We used metagenomes from Korean populations in this study. The dataset consists of three different types of samples, viz. mucosal tissue and stool from Crohn’s disease patients and stool from healthy individuals. We use the split graph model to analyze the impact of microbial compositions on various host phenotypes. Utilizing the graph model, we have developed a pipeline that integrates genomic information and pathway analysis to characterize both critical informative components of inter-bacterial correlations and associations between bacterial taxa and various metabolic pathways.ResultsThe obtained results highlight the importance of the microbial communities and their inter-relationships and show how these microbial structures are correlated with Crohn’s disease. We show that there are significant positive associations between detected taxonomic biomarkers as well as multiple functional modules in the split graph of mucosal tissue samples from CD patients. Bacteria Moraxellaceae and Pseudomonadaceae were detected as taxonomic biomarkers in CD groups. Higher abundance of these bacteria have been reported in previous study and several metabolic pathways associated with these bacteria were characterized in CD samples.ConclusionsThe proposed pipeline provides a new way to approach the analysis of complex microbiomes. The results obtained from this study show great potential in unraveling mechansims in complex biological systems to understand how various components in such complex environments are associated with critical biological functions.

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Polyamines in Gut Inflammation and Allergy

Cited by 10 publications

References 0 publications

Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines

Lactobacillus GG restoration of the gliadin induced epithelial barrier disruption: the role of cellular polyamines

Eukaryotic Translation Initiation Factor 5A Small Interference RNA–Liposome Complexes Reduce Inflammation and Increase Survival in Murine Models of Severe Sepsis and Acute Lung Injury

A novel graph theoretical approach for modeling microbiomes and inferring microbial ecological relationships

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