Disease ⇒ Colitis {40000146}

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] [#Crohn’s disease, #Inflamatory bowel disease] [#Saccharomyces cerevisiae] 
  - S cerevisiae has demonstrated anti-inflammatory effects against colitis in murine models - IBD patients and patients in flare present significantly less S cerevisiae. - mucosal-associated fungal studies have demonstrated an increase of S cerevisiae in noninflamed mucosa in CD patients
• [#Ulcerative Colitis] - decreasing abundance of #Penicillium from UC proctitis to extensive colitis, in which it virtually disappears > at species level (P. glandicola, P. roqueforti, P. citrinum, P. clavigerum, P. chrysogenum, and P. oxalicum) > an inverse correlation of #Penicillium and disease extension is described in UC.
• [#Saccharomyces pastorianus] - a combination of yeasts that included S pastorianus has showed promising anti-inflammatory results in a mice model of colitis
• - #Indole and its derivatives seem to increase the integrity of the epithelial barrier and function of tight junctions > reduce colitis related to #Citrobacter rodentium and #Candida albicans infection
• [1.31] [#Inflamatory bowel disease] [#Tryptophan] 
  - Trp metabolites XA and KA have been negatively correlated to inflammation not only in colitis mice models but also in humans with IBD.
• [1.32] [#Lactobacillus plantarum] 
  - L. plantarum Δbsh 1 and Δbsh 3 treatments did not improve body weight and alleviate the hyperactivated myeloperoxidase activity to the DSS group.
• [1.33] 
  - during chronic or intermittent dietary fiber deficiency, the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to erosion of the colonic mucus barrier. Dietary fiber deprivation, together with a fiber-deprived, mucus-eroding microbiota, promotes greater epithelial access and lethal colitis by the mucosal pathogen, #Citrobacter rodentium.
• [1.34] [#Inflamatory bowel disease] 
  - #Curcumin appears to promote colonic Treg cell expansion while decreasing the counts of inflammatory DCs; inhibiting pro-inflammatory cytokines’ secretion, T cell infiltration and NF-kB activation, as well as to suppress macrophage activation and regulate M1/M2 polarization
• [#Inflamatory bowel disease] - In humans, consumption of #Mango by IBD patients significantly improved Simple Clinical Colitis Activity Index (SCCAI) score and decreased the plasma levels of pro-inflammatory cytokines related to neutrophil-induced inflammation
• - lignan #Arctigenin inhibits Th17 and Th1 differentiation in vitro by repressing STAT3 and STAT4 phosphorylation respectively through mTORC1 downregulation, ameliorating DSS-induced colitis in mice
• - #Chlorogenic acid has also shown to mitigate DSS-induced colitis in mice by inhibiting M1 macrophage polarization through suppressing PKM2-dependent glycolysis and Nod-like receptor protein 3 activation
• - #Flavonoid #Galangin has shown to alleviate DSS-induced colitis’ symptoms in mice by increasing the expression of autophagy-related proteins and promoting colonic autophagosome formation
• [#Polyphenols, #Shikonin ] - shikonin – a polyphenol widely used in Chinese traditional medicine – has shown to suppress #Glucose consumption and #Lactate production as well as inhibit the nuclear translocation and enzymatic activity of PKM2, which is responsible for stimulating the Warburg effect in macrophages, in a DSS-induced colitis mouse model
• - #Resveratrol and #Resveratrol-related PCs (e.g. pterostilbene) have further demonstrated to alleviate intestinal inflammation in mice with colitis by regulating the Th17/Treg balance and control the levels of plasmatic and intestinal mucosal cytokines such as transforming growth factor beta (TGF-β), #IL-6, #IL-10 and #IL-17, restoring the percentage of CD4+ T cells in mesenteric lymph nodes (MLNs) and decrease their number in the intestinal LP, as well as reducing the percentage of macrophages in both regions
• [1.35] 
  - #Desulfovibrio are #Sulfate-reducing bacteria have the ability to reduce #Sulfate to #Hydrogen sulfide, which, when accumulated, can lead to damage to the intestinal epithelium, causing chronic inflammation and disrupting the balance between cellular proliferation and apoptosis
• [1.36] [#Crohn’s disease] [#Clostridioides difficile, #Clostridium paraputrificum] [#Fecal Microbiota Transplantation] 
  - Transferred fecal microbiota from healthy patients and patients with defined Crohn’s ileocolitis (CD_L3) to germ-free mice > a markedly reduced engraftment of CD_L3 microbiome compared to healthy control microbiota. - FMT from CD_L3 patients did not lead to ileitis but resulted in colitis with features consistent with CD: a discontinued pattern of colitis, more proximal colonic localization, enlarged isolated lymphoid follicles and/or tertiary lymphoid organ neogenesis, and a transcriptomic pattern consistent with epithelial reprograming and promotion of the Paneth cell-like signature in the proximal colon and immune dysregulation characteristic of CD. - The observed inflammatory response associated with persistently increased abundance of #Ruminococcus gnavus, #Erysipelatoclostridium ramosum, #Faecalimonas umbilicate, #Blautia hominis, #Clostridium butyricum, and C. paraputrificum and unexpected growth of toxigenic C. difficile.
• [1.37] 
  - red #Cabbage juice (RCJ) alleviates Dextran Sodium #Sulfate (DSS)-induced colitis in mice. - RCJ improved colonic barrier integrity by enhancing the expression of protective colonic mucinsand tight junction proteins in RCJ + DSS-treated mice compared to the DSS group. -RCJ enrichment of short-chain fatty acids (SCFAs)-producing bacteria, leading to increased Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) activation > resulted in repression of the nuclear factor κB (NFκB) signaling pathway, causing decreased production of inflammatory cytokines and chemokines.
• [1.38] [#Lactobacillus plantarum] 
  - treatment with #Lactobacillus plantarum L137 increased the abundance of #Lactobacillus species, improved intestinal barrier integrity via upregulation of #ZO-1, as well as modulated cytokine levels. - In colitis mice, treatment with #Lactobacillus plantarum L137 ameliorated disease-associated changes and exhibited an anti-inflammatory effect.
• [1.39] [#Inflamatory bowel disease] 
  - the promoter of #Polysaccharide A (PSA) of #Bacteroides fragilis, which induces regulatory T cells (Tregs) and ameliorates experimental colitis was mostly oriented “OFF” in IBD patients, which correlated with increased B. fragilis-associated bacteriophages. - in mice colonized with a healthy human microbiota and B. fragilis, induction of colitis caused a decline of PSA in the “ON” orientation that reversed as inflammation resolved. - Monocolonization of mice with B. fragilis revealed that bacteriophage infection increased the frequency of PSA in the “OFF” orientation, causing reduced PSA expression and decreased Treg cells.
• - #Akkermansia muciniphila and #Parabacteroides distasonis were significantly increased in the microbiota of resistant mice. - A. muciniphila and P. distasonis synergistically drive a protective effect in both acute and chronic models of colitis by boosting the frequency of type 3 innate lymphoid cells in the colon and by improving gut epithelial integrity.
• [1.41] [#Antibiotic Therapy] 
  - #Guar gum containing diet (GuD) increased the susceptibility to colonic inflammation. - Amelioration of colitis in GuD-fed group pre-treated with antibiotics suggest a vital role of intestinal microbiota in GuD-mediated exacerbation of intestinal inflammation.
• [1.42] [#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