Disease ⇒ Colitis {40000146}

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Shared Reference Notes

  • [1.1] [#Food colorants
    -Colitis induction was dependent on the commensal microbiota such as B. ovatus and E. faecalis promoting the azo reduction of Red 40 and generation of a metabolite, 1-amino-2-naphthol-6-sulfonate sodium salt.
  • [1.2] [#Colorectal cancer, #Crohn’s disease, #Inflamatory bowel disease] [#Common consumer products
    - #Triclosan (TCS), an antimicrobial agent found in thousands of consumer products > exacerbates colitis and colitis-associated colorectal tumorigenesis in animal models. - intestinal commensal microbes > microbial β-glucuronidase (GUS) enzymes > mediate metabolic activation of #Triclosan in the colon > gut toxicology.
  • [1.3] [#Crohn’s disease] [#Candida tropicalis
    - C. tropicalis > induces dysbiosis that involves changes in the presence of mucin-degrading bacteria #Akkermansia muciniphila and #Ruminococcus gnavus > leading to altered tight junction protein expression with increased intestinal permeability > followed by induction of robust Th1/Th17 responses > lead to an accelerated proinflammatory phenotype in experimental colitic mice.
  • [1.4
    - Brain’s insular cortex (InsCtx) stores immune-related information. - Chemogenetic reactivation of these neuronal ensembles > broadly retrieve the inflammatory state under which these neurons were captured.
  • [1.5
  • [1.6
    - Oral gavages of #Klebsiella oxytoca, #Escherichia coli, and #Cronobacter sakazakii belonging to Enterobacteriaceae, singly or together, caused dose-dependently colitis and #Depression-like behaviors in germ-free and specific-pathogen-free mice.
  • [1.7] [#Hypertension] [#High salt diet
    - Salt consumption decreased #Lactobacillus abundance, which was linked to increased T helper 17 cell numbers in murine small intestinal lamina propria lymphocytes and human peripheral blood lymphocytes, as well as higher blood pressure. - a high-salt diet reduced #Lactobacillus abundance, increased proinflammatory gene expression, and exacerbated colitis in two separate disease models
  • [1.8] [#Inflamatory bowel disease
    - #Psyllium, a fiber derived from Plantago seeds, can inhibit #inflammation that leads to Colitis in mice by increasing serum #Bile Acids and activating the farnesoid X receptor (FXR). - This is exciting since it suggests that pharmacologic FXR activation might be an interesting target for the management of inflammation found in IBD.
  • [1.9
    - 3,8-Dihydroxy-urolithin (#Urolithin A), a metabolite of #Ellagic acid which is found in high levels in pomegranate, acts on the #AHR and nuclear factor erythroid 2–related factor 2 (NRF2) signalling pathways to upregulate the expression of TJs proteins and ameliorate colitis - #Urolithin A is an agonist of #AHR able to reduce the expression of inflammatory genes.
  • [#Clostridium difficile associated disease] -#Bile Salt hydrolases (BSH) enzymes can restrict the growth of the deadly colitis-inducing bacterium #Clostridioides difficile.
  • [1.11] [#Ulcerative Colitis] [#Lactobacillus mucosae
    - In ulcerative colitis, excessive epithelial repair results in lower PPAR-γ synthesis, which reduces beta-oxidation and increases oxygenation of colonocytes. Inflamed mucosae in colitis patients are increased in #Proteobacteria, a major phylum of gram-negative bacteria, but decreased in gram-positive #Firmicutes. Treatment with PPAR-γ agonist, however, can improve the microbial balance
  • [1.12
    - In acute colitis, #Melatonin led to increased clinical, systemic and intestinal inflammatory parameters. - During remission, continued MLT administration delayed recovery, increased TNF, memory effector lymphocytes and diminished spleen regulatory cells. - MLT treatment reduced #Bacteroidetes and augmented #Actinobacteria and #Verrucomicrobia phyla in mice feces. - Microbiota depletion resulted in a remarkable reversion of the colitis phenotype after MLT administration, including a counter-regulatory immune response, reduction in TNF and colon macrophages. - There was a decrease in #Actinobacteria, #Firmicutes and, most strikingly, #Verrucomicrobia phylum in recovering mice. Finally, these results pointed to a gut-microbiota-dependent effect of MLT in the potentiation of intestinal inflammation.
  • [1.13] [#Palmitoleic acid
    - co-administration of POA with #Akkermansia muciniphila showed significant synergistic protections against colitis in mice.
  • [1.14] [#Allura Red AC
    - chronic exposure of AR at a dose found in commonly consumed dietary products exacerbates experimental models of colitis in mice. - chronic exposure to AR induces mild colitis, which is associated with elevated colonic serotonin (5-hydroxytryptamine; 5-HT) levels and impairment of the epithelial barrier function via myosin light chain kinase (MLCK). - intermittent exposure to AR in mice for 12 weeks, does not influence susceptibility to colitis. - exposure to AR during early life primes mice to heightened susceptibility to colitis. - Cecal transfer of the perturbed gut microbiota by AR exposure worsens colitis severity in the recipient germ-free (GF) mice. - chronic AR exposure elevates colonic 5-HT levels in naïve GF mice.
  • [1.15] [#Crohn’s disease
    - Colonization with CD-high fecal proteolytic activityled (CD-HPA) to a spontaneous proinflammatory immune tone and worsened experimental colitis in wild type and Nod2−/- mice, but not in mice with a PAR2 mutation that makes it resistant to cleavage by proteases, indicating the proinflammatory pathway requires intact PAR2 cleavage signaling.
  • [#Crohn’s disease] - opportunistic pathogens were increased in CD-HPA colonized mice, such as #Romboutsia ilealis, that has been reported to be increased in an experimental colitis model.
  • [1.16] [#Crohn’s disease
    - Administration of PAGly exacerbated colitis in mouse model and upregulated coagulation-related biological processes. - High dietary protein intake and increased abundance of #Phenylacetic acid (PAA)-producing #Proteobacteria mediated by phenylpyruvate decarboxylase act in concert to cause the elevated PAGln levels in CD patients.
  • [1.17] [#Colorectal cancer
    - Certain strains of #Bacteroides fragilis, a known intestinal symbiont, have been shown to up-regulate Wnt/B-catenin and NF–KB signaling in chronic colitis and CRC tissue. - These strains secrete a specific exotoxin, associated with increased pro-inflammatory Th17 T-cell activity, promoting cell survival
  • [1.18] [#Escherichia coli
    - #Vitamin B12 supplementation in mice significantly decreased #Parabacteroides and #Lactobacillus and increased E. coli and #Enterococcus abundances in a murine model of colitis
  • [1.19] [#Short Chain Fatty Acid
    - Combination of SCFAs, mainly #Acetate, #Propionate, and #Butyrate, showed increased effects against colitis
  • - A mixture of #Butyrate, Pistacia atlantica, and #Lactobacillus casei or #Butyrate, #Lactobacillus casei, and L-carnitin showed synergistic effects than a single agent in a TNBS-induced rat colitis model
  • [#Eubacterium limosum, #Roseomonas mucosa] - E. limosum can reduce colitis, and the metabolite #Butyrate can enhance the integrity of the mucosa and show anti-inflammatory regulation on the intestinal mucosal system through Toll-like receptor 4 (TLR4)
  • [1.21] [#Lactobacillus plantarum
    - L. plantarum administration reduced the incidence of DSS-induced colitis. L. plantarum uptake maintained the integrity and permeability of intestinal epithelial cells and increased mucin secretion from goblet cells.
  • [1.22] [#Faecalibacterium prausnitzii] [#Immune checkpoint inhibitor
    - patients receiving ICIs who developed colitis had a lower abundance of F. prausnitzii. - F. prausnitzii administration mitigated the exacerbated colitis induced by ICIs. - F. prausnitzii enhanced the anti-tumor immunity elicited by ICIs in tumor-bearing mice while abrogating colitis. - administration of F. prausnitzii increased gut microbial alpha diversity and modulated the microbial composition, increasing a subset of gut probiotics and decreasing potential gut pathogens. - F. prausnitzii abundance was reduced in mice that developed ICI-associated colitis.
  • [1.23] [#Inflamatory bowel disease] [#β-hydroxybutyrate
    -BHB alleviates intestinal inflammation in DSS-induced colitis, which could be due to its ability to promote M2 macrophage polarization. - locally BHB levels are negatively correlated with the severity of DSS-induced colitis and human IBD. - BHB treatment lead to significantly increased expression of M2-associated genes in DSS-exposed colons. - BHB facilitates mucosal repair through promoting intestinal epithelial proliferation in murine IBD. - BHB-treated mice had less crypt loss and epithelium damage in the DSS-exposed colons. - BHB increased the expression of bromodeoxyuridine (Brdu) and proliferating cell nuclear antigen (PCNA), two cell proliferation markers, in the DSS-exposed colons. - exogenous BHB supplement exerts anti-aging effect on intestinal stem cells by reducing oxidative stress-induced DNA damage accumulation
  • [1.24] [#Deoxycholic acid
    - In a mouse model, DCA supplementation increased oxidative damage in colonic epithelium
  • [1.25
    - macrophages produce large amounts of the polyamines spermidine and #Spermine via the mTORC1 signaling pathway. - These polyamines were taken up by the epithelial cells, leading to a switch in their cell metabolism, promoting their proliferation and strengthening their defense mechanisms. - #Spermine in particular had a major stimulatory effect on the proliferation of colon cells. I - this mTORC1 activation and #Polyamine production had a protective effect against inflammatory bowel injury in animal models. - Polyamines especially spermidine have been heavily researched for some time as studies show that these substances can prolong life and slow down the aging process.
  • [1.26] [#Hydrogen sulfide
    - increased #Sulfate-reducing bacteria, thereby increasing bacterially derived H2S levels, increased Th17- and T regulatory-cell-type cytokine production and activation profiles in mesenteric lymph nodes in experimental colitis
  • [#Para-cresol] - When p-cresol presents in excess in colonocytes, it inhibits mitochondrial #Oxygen consumption and consequently reduces cell proliferation. - when colonocytes were treated with p-cresol, anion superoxide production and DNA-double strand break were increased; thus, p-cresol is genotoxic.
  • [1.27
    - #Bacteroides fragilis also were found to protect mice from infection with #Helicobacter hepaticus and colitis induced by trinitrobenzene sulfonic acid (TNBS)
  • [1.28] [#Antimicrobial peptides
    - #Lysozyme, the major AMP, can directly reduce the propagation of #Reactive Oxygen Species in colitis by releasing bacterial #Superoxide dismutase from #Lactobacillus lactis
  • [1.29] [#Diabetes Type 1
    - The protein expressed by the #Bacteroides is almost identical to a protein expressed by insulin-producing cells in the pancreas. - The CD8 lymphocytes can mistakenly attack the pancreatic cells and cause type 1 diabetes.

References Notes

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