Abstract:The intestinal mucus is a pivotal part of our intestinal protection. It provides slow diffusion of protective molecules, trapping of luminal material as bacteria and smooth transport in the small intestine. In colon it restricts bacterial access to the epithelium limiting the responses to the enormous bacterial load present at this location. The development of these systems depends on the microbiota composition as seen in our recent study comparing the mucus phenotype in 2 colonies kept in different husbandrie… Show more
“…From our analysis of microbiome and metabolome, we could propose some ways through which bacteria affect kidney damage. For instance, it was shown that bacteria play a "nephroprotective" role (Prevotella copri [43], Faecalibacterium prausnitzii [44,45], and Coprococcus eutactus [46]), being reversely associated with the severity of AKI, and are known to produce short-chain fatty acids (SCFAs), mainly represented by acetate, propionate, and butyrate [47]. Most of these molecules (especially butyrate) are used by the intestine epithelium as an energy source, however, a fraction of these goes into the bloodstream, and then transfer to the organs, inhibiting the histone deacetylase activity [48].…”
Intestinal microbiota play a considerable role in the host’s organism, broadly affecting its organs and tissues. The kidney can also be the target of the microbiome and its metabolites (especially short-chain fatty acids), which can influence renal tissue, both by direct action and through modulation of the immune response. This impact is crucial, especially during kidney injury, because the modulation of inflammation or reparative processes could affect the severity of the resulting damage or recovery of kidney function. In this study, we compared the composition of rat gut microbiota with its outcome, in experimental acute ischemic kidney injury and named the bacterial taxa that play putatively negative or positive roles in the progression of ischemic kidney injury. We investigated the link between serum creatinine, urea, and a number of metabolites (acylcarnitines and amino acids), and the relative abundance of various bacterial taxa in rat feces. Our analysis revealed an increase in levels of 32 acylcarnitines in serum, after renal ischemia/reperfusion and correlation with creatinine and urea, while levels of three amino acids (tyrosine, tryptophan, and proline) had decreased. We detected associations between bacterial abundance and metabolite levels, using a compositionality-aware approach—Rothia and Staphylococcus levels were positively associated with creatinine and urea levels, respectively. Our findings indicate that the gut microbial community contains specific members whose presence might ameliorate or, on the contrary, aggravate ischemic kidney injury. These bacterial taxa could present perspective targets for therapeutical interventions in kidney pathologies, including acute kidney injury.
“…From our analysis of microbiome and metabolome, we could propose some ways through which bacteria affect kidney damage. For instance, it was shown that bacteria play a "nephroprotective" role (Prevotella copri [43], Faecalibacterium prausnitzii [44,45], and Coprococcus eutactus [46]), being reversely associated with the severity of AKI, and are known to produce short-chain fatty acids (SCFAs), mainly represented by acetate, propionate, and butyrate [47]. Most of these molecules (especially butyrate) are used by the intestine epithelium as an energy source, however, a fraction of these goes into the bloodstream, and then transfer to the organs, inhibiting the histone deacetylase activity [48].…”
Intestinal microbiota play a considerable role in the host’s organism, broadly affecting its organs and tissues. The kidney can also be the target of the microbiome and its metabolites (especially short-chain fatty acids), which can influence renal tissue, both by direct action and through modulation of the immune response. This impact is crucial, especially during kidney injury, because the modulation of inflammation or reparative processes could affect the severity of the resulting damage or recovery of kidney function. In this study, we compared the composition of rat gut microbiota with its outcome, in experimental acute ischemic kidney injury and named the bacterial taxa that play putatively negative or positive roles in the progression of ischemic kidney injury. We investigated the link between serum creatinine, urea, and a number of metabolites (acylcarnitines and amino acids), and the relative abundance of various bacterial taxa in rat feces. Our analysis revealed an increase in levels of 32 acylcarnitines in serum, after renal ischemia/reperfusion and correlation with creatinine and urea, while levels of three amino acids (tyrosine, tryptophan, and proline) had decreased. We detected associations between bacterial abundance and metabolite levels, using a compositionality-aware approach—Rothia and Staphylococcus levels were positively associated with creatinine and urea levels, respectively. Our findings indicate that the gut microbial community contains specific members whose presence might ameliorate or, on the contrary, aggravate ischemic kidney injury. These bacterial taxa could present perspective targets for therapeutical interventions in kidney pathologies, including acute kidney injury.
“…In the liver, we identified 222 proteins, of which 58 proteins were downregulated and 75 proteins were upregulated in DSSWOL compared to the DSS group (Supplementary Table 3). WOL supplementation decreased the levels of proteins that are known to be commonly upregulated in IBD patients: calreticulin (Calr) 33 , serotransferrin (Trfe) 34 , annexin A5 (Anxa5) 35 , beta-enolase (Enob) 36 , transthyretin (Tthy) 37 , selenium-binding protein 1 (Sbp1) 38 , and protein-glutamine gamma-glutamyltransferase 2 (Tgm2) 39 ; proteins involved in fibrosis: fibrinogen beta chain (Fibb) and fibrinogen gamma chain (Fibg) 40 ; and inflammation-related proteins: histone H4 (H4), superoxide dismutase [Cu-Zn] (Sodc) 41 , cystatin-B (Cytb) 42 , 10-kDa heat shock protein, mitochondrial (Ch10) 43 , thioredoxin (Thio) 44 , and alpha-enolase (Enoa) 45 .…”
Section: Comparative Hepatic and Colonic Proteomics Analysis By Itraqmentioning
We used a multi-omics profiling approach to investigate the suppressive effects of 2% Wolfberry (WOL)-enriched diets on dextran sodium sulfate (DSS)-induced colitis in mice. It was observed that in mice fed the WOL diet, the disease activity index, colon shortening, plasma concentrations of matrix metalloproteinase-3 and relative mesenteric fat weight were significantly improved as compared to the DSS group. Results from colon transcriptome and proteome profiles showed that WOL supplementation significantly ameliorated the expression of genes and proteins associated with the integrity of the colonic mucosal wall and colonic inflammation. Based on the hepatic transcriptome, proteome and metabolome data, genes involved in fatty acid metabolism, proteins involved in inflammation and metabolites related to glycolysis were downregulated in WOL mice, leading to lowered inflammation and changes in these molecules may have led to improvement in body weight loss. The integrated nutrigenomic approach thus revealed the molecular mechanisms underlying the ameliorative effect of whole WOL fruit consumption on inflammatory bowel disease.
“…Consistently, while several reports support a causal relevance for Akkermansia in improving metabolic phenotypes 2,26,35,36 , molecules of microbial origin were shown to stimulate mucus release 37 and the composition of the gut microbiota plays a key role in the development of an impenetrable mucus layer. 38 In addition, Akkermansia has been shown to fortify in vitro the integrity of the epithelial cell layer, suggesting that the positive role of this bacterium in the gut barrier is not exclusively associated with mucus layer physiology. 39 An important question is whether administration of Akkermansia should be regarded as a safe approach to prevent or even reverse metabolic diseases.…”
Section: Is Akkermansia a New Bacterial Weapon To Fight Chronic Inflamentioning
The gut and its bacterial colonizers are now well characterized as key players in whole-body metabolism, opening new avenues of research and generating great expectation for new treatments against obesity and its cardiometabolic complications. As diet is the main environmental factor affecting the gut microbiota, it has been suggested that fruits and vegetables, whose consumption is strongly associated with a healthy lifestyle, may carry phytochemicals that could help maintain intestinal homeostasis and metabolic health. We recently demonstrated that oral administration of a cranberry extract rich in polyphenols prevented diet-induced obesity and several detrimental features of the metabolic syndrome in association with a remarkable increase in the abundance of the mucin-degrading bacterium Akkermansia in the gut microbiota of mice. This addendum provides an extended discussion in light of recent discoveries suggesting a mechanistic link between polyphenols and Akkermansia, also contemplating how this unique microorganism may be exploited to fight the metabolic syndrome.
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