Changes in intestinal microbiota and correlation with TLRs in ulcerative colitis in the coastal area of northern China

Atractylodin Attenuates Dextran Sulfate Sodium-Induced Colitis by Alleviating Gut Microbiota Dysbiosis and Inhibiting Inflammatory Response Through the MAPK Pathway

“…Proteobacteria is one of the larger bacterial communities, which includes several pathogenic bacteria, such as Escherichia coli, Salmonella, Vibrio cholerae, and Helicobacter pylori among others. The proportion of Proteobacteria in patients with ulcerative colitis is known to increase significantly (Xu et al, 2021). Adhesively invasive E. coli increased the abundance of Proteobacteria and Deferrobacter in a porcine model of experimental colitis and these findings were similar to that observed in patients with IBD (Munyaka et al, 2016).…”

Oscillospira - a candidate for the next-generation probiotics

“… 2 Xu et al found that Oscillospira abundance was negatively correlated with disease severity in patients with ulcerative colitis (UC). 119 Lima et al found a lower abundance of Oscillospira in the gut of children with inflammatory bowel disease (IBD). 120 A significantly lower abundance of Oscillospira was also found in the gut of Crohn’s disease (CD) patients and pediatric nonalcoholic fatty liver disease (NALD) patients.…”

Microbiota-Immune Interactions in Ulcerative Colitis and Colitis Associated Cancer and Emerging Microbiota-Based Therapies

“…For example, the microbiome in UC is characterized by reduced bacterial α-diversity, reflecting species richness and evenness, and β-diversity (variability) in community composition between UC and healthy subjects [71,72]. UC is associated with a decrease in the number of bacterial taxa from the Firmicutes and Bacteroidetes phyla and a significant increase in bacterial communities from the Proteobacteria phylum [71][72][73][74][75]. These changes are collectively described as a state of bacterial dysbiosis.…”

“…This dysbiosis could explain the presence of inflammation in the colon of UC patients, as the increased abundance of Gram-negative taxa such as Escherichia-Shigella, Fusobacterium, Actinobacillus, Streptococcus, and Campylobacter shift the host-microbe equilibrium towards a proinflammatory phenotype, supported by evidence of altered expression of several TLRs in subjects with UC [76][77][78]. TLR4 recognizes molecular profiles derived from Gram-negative bacteria (i.e., lipopolysaccharide), thus, playing a key role in limiting their invasion when the intestinal barrier is disrupted during inflammation [75]. Conversely, the depletion of members from the Clostridiaceae family (phylum Firmicutes), such as Faecalibacterium prausnitzii and other species from the genera Clostridium, Ruminococcus, Eubacterium, Roseburia, and Akkermansia significantly lower production of butyrate, propionate, and acetate, and thus impair epithelial barrier function by reducing colonocyte proliferation and affecting Treg cells' maturation through abnormal production of proinflammatory markers [20,71,72,[79][80][81].…”

“…Conversely, the depletion of members from the Clostridiaceae family (phylum Firmicutes), such as Faecalibacterium prausnitzii and other species from the genera Clostridium, Ruminococcus, Eubacterium, Roseburia, and Akkermansia significantly lower production of butyrate, propionate, and acetate, and thus impair epithelial barrier function by reducing colonocyte proliferation and affecting Treg cells' maturation through abnormal production of proinflammatory markers [20,71,72,[79][80][81]. Fusobacteria ↑tumorigenesis in the colon [72] Faecalibacterium prausnitzii ↑production of IL-12, IFNγ and reduction of IL-10 levels in blood cells [85] Adlercreutzia ↓synthesis of isoflavones, phenolic compounds with antimicrobial and anti-inflammatory properties [78] Ruminococcus bromii, Eubacterium rectale, Roseburia, and Akkermansia ↓butyrate production = impaired epithelial barrier function ↑epithelial permeability and commensals translocation [20,71,72] ↑colonic inflammation with crypt abscess [84] ↑of deciduous epithelial and/or blood cells in stools of patients with UC or CAC, gut barrier injury, impaired cell cycle [82] ↑Proteobacteria [20,[70][71][72]75] Families ↓Clostridiaceae [71,72] ↑Enterobacteriaceae [86] Genera [70] ↑β-diversity between UC in flare as compared with UC in remission and to HC [70] ↑ ratio of Basidiomycota/Ascomycota in UC in flare as compared with UC in remission and to HC [70] ↑correlation between fungi and bacteria in UC as compared with CD and HC [70] Colonic mucosa: ↓fungi load in UC as compared with HC No significant changes in α-diversity UC mycobiota clusters differently from HC No changes in the ratio of Basidiomycota/Ascomycota [88] N/A…”