Arabinoxylans, inulin and Lactobacillus reuteri 1063 repress the adherent-invasive Escherichia coli from mucus in a mucosa-comprising gut model
http://www.nature.com/articles/npjb...Microbiomes)&utm_content=Google+International
Are there any other ways to manipulate AIEC in Crohn's patients? Does vitamin d supplementation have any effect? In theory it should:
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VDR/vitamin D receptor regulates autophagic activity through ATG16L1.
https://www.ncbi.nlm.nih.gov/pubmed/26218741
Vitamin D deficiency enhances adherent invasive Escherichia coli induced barrier dysfunction and experimental colonic injury
https://www.ecco-ibd.eu/index.php/p...function-and-experimental-colonic-injury.html
Figure: Vitamin D enhances intramacrophage killing of AIEC. 1,25 OH2-vitamin D3 caused dose-dependent decrease in intramacrophage survival of AIEC HM605 in (A) J774A.1 murine macrophages (N = 3, Cuzick\'s test for trend; P < 0.001) and (B) human MDM (N = 3, Cuzick\'s test; P = 0.012). *P < 0.05, ***P < 0.001 Dunnett\'s test versus control.
Nutritional Management of Inflammatory Bowel Diseases: A Comprehensive Guide
https://books.google.com.tr/books?i...AQ6AEINDAD#v=onepage&q=AIEC vitamin d&f=false
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What about other ways? Can we manipulate AIEC through dietary interventions? Like reducing certain kind of carbohydrates, or any specific micronutrients affecting it?
http://www.nature.com/articles/npjb...Microbiomes)&utm_content=Google+International
How would it turn out in vivo? To begin with, are probiotics (and prebiotics) even safe for Crohn's patients (who have intestinal permeability dysfunction)? I always stay away from probiotics-prebiotics because of this reason; even on antibiotics I don't take them....L. reuteri 1063, LC-AX and IN specifically lowered AIEC numbers in the simulated mucosal environment of the M-SHIME, while they did not affect AIEC numbers in the luminal content. As a possible explanation, supplementation of IN and LC-AX (during 8 days prior to AIEC inoculation) altered the resident mucosal microbiota, especially subdominant groups (lactobacilli and bifidobacteria). Not only did LC-AX and IN increase the mucosal counts of lactobacilli and bifidobacteria, they also altered the species composition of the bifidobacteria. As shown by DGGE, initially the dominant mucosal Bifidobacterium species was B. bifidum, IN specifically stimulated B. adolescentis in mucus and LC-AX specifically stimulated both B. longum and B. adolescentis in mucus. B. longum has been shown to possess a stronger antimicrobial activity against Escherichia coli compared with B. bifidum.26 Also B. adolescentis was shown to be very effective in combating Escherichia coli compared with B. bifidum27 but also compared with many other Bifidobacterium and Lactobacillus species.28 While antimicrobial factors are possibly too diluted in the intestinal content to be effective, the mucosal environment may allow trapping of antimicrobial factors, thereby repressing AIEC. Especially the spatial heterogeneity introduced by the biofilm on top of the mucin layer may result in local accumulation of e.g., acids produced by lactobacilli or bifidobacteria.
...In conclusion, we showed that the M-SHIME technology—using mucin-covered microcosms—provided a detailed insight in the long-term in vitro microbial colonisation of AIEC, an opportunistic pathogen and abundant mucosal microbe. Moreover, it allowed to evaluate the colonisation of a simulated mucus layer in the presence of a resident mucosal and luminal intestinal microbiota. It has to be considered that in this type of studies, the relevance of the data in terms of potential interindividual variability (i.e., different effect of the test products due to a different composition of the gut microbiota) may be questionable. Our aim was to present a technology platform that might be applied on other disease-causing microbes such as food-borne pathogens and to provide evidences on the potential of several pre- and probiotic strategies to repress AIEC from the mucosal compartment. Here we showed—with the microbiota from one donor—that such repression may occur via different mechanisms including the production of reuterin, undissociated lactic acid or adhesion inhibition. The evaluation of the role of the microbiota from different donors on these mechanisms can be an interesting future line of research. We also showed that the incorporation of a mucosal environment in dynamic gut models may be a powerful tool to obtain a more realistic view on processes that drive the gastrointestinal microbiome.
Are there any other ways to manipulate AIEC in Crohn's patients? Does vitamin d supplementation have any effect? In theory it should:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133521/Once inside the host cell, LF82 bacteria can be found in several types of intracellular compartments: individually or in groups within single membrane vacuoles, within damaged vacuoles, or within LC3-positive autophagosomes, which indicates that autophagy restricts a subpopulation of intracellular LF82 bacteria[57]. Nevertheless, it was recently demonstrated that AIEC can abrogate the autophagic process[58]. Intracellular LF82 activates NF-κB, leading to the increased expression of MIR30C and MIR130A in T84 cells and in mouse enterocytes, and the upregulation of these microRNAs reduces levels of ATG5 and ATG16L1, inhibiting autophagy and enhancing the inflammatory response. In turn, defects in autophagy mechanisms related to the ATG16L1 and IRGM genes have been associated with CD patients, and these defects confer an advantage for AIEC to survive inside human cells[57]. Therefore, it is a combination of host deficiency factors and AIEC pathogenicity that determines the fate of intracellular E. coli survival.
*******
VDR/vitamin D receptor regulates autophagic activity through ATG16L1.
https://www.ncbi.nlm.nih.gov/pubmed/26218741
Vitamin D deficiency enhances adherent invasive Escherichia coli induced barrier dysfunction and experimental colonic injury
https://www.ecco-ibd.eu/index.php/p...function-and-experimental-colonic-injury.html
Figure: Vitamin D enhances intramacrophage killing of AIEC. 1,25 OH2-vitamin D3 caused dose-dependent decrease in intramacrophage survival of AIEC HM605 in (A) J774A.1 murine macrophages (N = 3, Cuzick\'s test for trend; P < 0.001) and (B) human MDM (N = 3, Cuzick\'s test; P = 0.012). *P < 0.05, ***P < 0.001 Dunnett\'s test versus control.
Nutritional Management of Inflammatory Bowel Diseases: A Comprehensive Guide
https://books.google.com.tr/books?i...AQ6AEINDAD#v=onepage&q=AIEC vitamin d&f=false
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What about other ways? Can we manipulate AIEC through dietary interventions? Like reducing certain kind of carbohydrates, or any specific micronutrients affecting it?