Microbiome & Chronic Diseases

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Disease ⇒ Irritable bowel syndrome {40000135}

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Irritable bowel syndrome
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- Oral administration of Bifidobacterium infantis 35624 normalized sensitivity to colorectal distension in a rat model of post-inflammatory colonic hypersensitivity (1)

- The probiotic B. infantis 35624 reduced CRD-induced visceral pain behaviors in both rat strains. It significantly increased the threshold pressure of the first pain behavior and also reduced the total number pain behaviors during CRD (2)

- Purine metabolism is the novel host-microbial metabolic pathway in IBS (4)

References Notes

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Shared Reference Notes

  • [1.24
    - Mice colonized with IBS+A microbiota developed faster gastrointestinal transit and anxiety‐like behavior (longer step‐down latency) compared to mice with HC microbiota.
    - Saccharomyces boulardii administration normalized gastrointestinal transit and anxiety‐like behavior in mice with IBS+A microbiota.

    Step‐down latency correlated with colonic Trpv1 expression and was associated with altered microbiota profile and increased Indole‐3‐acetic acid (IAA) levels.
  • [1.27
    - Individuals with severe IBS consumed a higher proportion of food items that can be considered as low quality (“less healthy”) as part of their main meals.
    - IBS severity is associated with altered gut microbiota hydrogen function in correlation with microbiota enzymes involved in animal carbohydrate metabolism.
  • [1.28
    - Staphylococcal bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine.
    - Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain.
    -This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents.
    - Injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation.
  • [1.29
    - Streptococci and clostridia were associated with an increased risk.
    - Clostridium perfringens is a well-known enteric pathogen and streptococci have been previously associated with irritable bowel syndrome.
    - Demographic risk factors included a family history of irritable bowel syndrome and antibiotic use.
    - Half of those affected said that their parents or siblings had bowel disease, and 75% of those affected said they had taken antibiotics in the past year.
  • [1.30
    - Patients had a significant improvement from baseline to 12 weeks in total percentage of bowel movements.
    - Improvement was similar across IBS subtypes. Symptoms improved most in the first 4 weeks of intervention.
    - The most common side effects were mild gastrointestinal symptoms such as flatulence, abdominal pain and discomfort, and distension.
  • [1.32
    - Irritable bowel syndrome patients had lower urinary Phosphatidyl choline acyl-alkyl C38:6, dopamine and p-hydroxybenzoic acid.
    - Levels of some urinary metabolites including histamine correlated significantly with irritable bowel syndrome symptom severity scores.
  • [1.33
    - Combining human variables and gut microbiota achieved the best performances in predicting IBD, IBS, CDI, and unhealthy status, indicating independent associations between gut microbiota and these diseases.
  • [1.20
    - In IBS > The three most abundant bacteriophage clusters belonged to the Siphoviridae, Myoviridae, and Podoviridae families (Order Caudovirales).
  • [1.25
    - In IBS patients, the GABAergic system is disrupted, and the levels of glutamate decarboxylase 2 (GAD2), GABA, and GABA receptors(including type B1 and B2) are decreased, while GABA transporter-2 (GAT-2) is increased in IBS-D patients
  • - histamine level in the colon was increased in IBS cases
  • -IBS > the level of neuroprotective kynurenic acid (KynA) and the ratio of KynA/Kyn were reduced
  • - Transplantation of feces from IBS-C patients to healthy mice would cause gut microbiota imbalance by reducing Firmicutes and increasing Bacteroides and Akkermansia.
    - the abundance of Bifidobacteria and Lactobacilli, as well as Enterobacteria was increased.
  • [1.34
    - Bifidobacterium infantis seems to be effective in human studies with IBS patients by changing plasma proinflammatory to anti-inflammatory cytokine ratio.

Common References