Gut dysbiosis and clinical phases of pancolitis in patients with ulcerative colitis

Maldonado-Arriaga, Brenda; Sandoval-Jiménez, Sergio; Rodrı́guez-Silverio, Juan; Alcaráz-Estrada, Sofía Lizeth; Cortés-Espinosa, Tomás; Vaca, Rebeca Pérez‐Cabeza de; Gámez-Valdez, July Stephany; Shaw, Jonathan G.; Mondragón‐Terán, Paul; Hernández-Cortez, Cecilia; Suárez‐Cuenca, Juan Antonio; Castro-Escarpulli, Graciela

doi:10.1002/mbo3.1181

Cited by 18 publications

(7 citation statements)

References 76 publications

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“…Certain Clostridium bacteria demonstrate pro-inflammatory properties by penetrating and mucosalizing the intestinal mucosa. Similarly, increasing bifidobacteria abundance has been shown to stimulate Th1 cell-mediated immune responses ( 83 ). Additionally, TLRs identification of bacterial and fungal surface components results in excessive activation of TLRs signaling pathways, triggering innate and adaptive immunity and chronic inflammation when the gut barrier is disrupted and pathogenic bacteria colonize.…”

Section: The Risk Factors With the Occurrence Of Ucmentioning

confidence: 99%

The Communication Between Intestinal Microbiota and Ulcerative Colitis: An Exploration of Pathogenesis, Animal Models, and Potential Therapeutic Strategies

et al. 2021

Front. Med.

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Ulcerative Colitis (UC) is a chronic inflammatory bowel disease. The prolonged course of UC and the lack of effective treatment management make it difficult to cure, affecting the health and life safety of patients. Although UC has received more attention, the etiology and pathogenesis of UC are still unclear. Therefore, it is urgent to establish an updated and comprehensive understanding of UC and explore effective treatment strategies. Notably, sufficient evidence shows that the intestinal microbiota plays an important role in the pathogenesis of UC, and the treating method aimed at improving the balance of the intestinal microbiota exhibits a therapeutic potential for UC. This article reviews the relationship between the genetic, immunological and microbial risk factors with UC. At the same time, the UC animal models related to intestinal microbiota dysbiosis induced by chemical drugs were evaluated. Finally, the potential value of the therapeutic strategies for restoring intestinal microbial homeostasis and treating UC were also investigated. Comprehensively, this study may help to carry out preclinical research, treatment theory and methods, and health management strategy of UC, and provide some theoretical basis for TCM in the treatment of UC.

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Section: The Risk Factors With the Occurrence Of Ucmentioning

confidence: 99%

The Communication Between Intestinal Microbiota and Ulcerative Colitis: An Exploration of Pathogenesis, Animal Models, and Potential Therapeutic Strategies

et al. 2021

Front. Med.

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“…Many studies have confirmed that intestinal microbiota imbalance is closely related to UC disease [ 27 ]. Therefore, a reduction in bacterial diversity has been verified in UC patients and animal models with colitis.…”

Section: Discussionmentioning

confidence: 99%

Saccharina japonica Ethanol Extract Ameliorates Dextran Sulfate Sodium-Induced Colitis via Reshaping Intestinal Microenvironment and Alleviating Inflammatory Response

Liu

Lin

et al. 2023

Foods

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Saccharina japonica belongs to brown macro-alga with various potential health benefits; its antioxidant and anti-inflammatory activities indicate the potential to improve inflammatory bowel diseases. Here, the potential anti-colitis effect of Saccharina japonica extract (SJE) was evaluated on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in C57B/L6 mice. The mice were treated with mesalazine (MES) and various doses of SJE by gavage for 14 days. Results showed that both MES and SJE treatment decreased the disease activity index scores, relieving the short colon. SJE increased the occludin and zonula occludens-1 levels, and the beneficial effects were better than MES. MES and SJE exerted similar effects in decreasing inflammatory cytokines and oxidative stress. Moreover, SJE reshaped the intestinal microbiota by increasing α-diversity and reducing plenty of harmful bacteria. Dietary SJE was significant to relieving the reduction in short-chain fatty acids. The results revealed the protective effect of SJE on colitis and potential mechanisms, which is important for the rational use of SJE in UC prevention.

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“…Notably, the present study found concordant data that after induction of UC using DSS, the proportion of Proteobacteria was significantly increased. 27 , 41 Moreover, prior research demonstrated a transiently unstable gut microbiota, especially a Proteobacteria-dominated community could predispose genetically susceptible mice to chronic colitis, as mice lacking Toll-like receptor-5 developed colitis and dysbiosis, which was associated with an abnormal expansion of Proteobacteria. 42 As for Patescibacteria, there were few reports on its role in UC.…”

Section: Discussionmentioning

confidence: 99%

Gancao Xiexin Decoction Ameliorates Ulcerative Colitis in Mice via Modulating Gut Microbiota and Metabolites

Luo¹,

Wu²,

Zhu³

et al. 2022

DDDT

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Purpose Ulcerative colitis (UC) is a chronic inflammatory bowel disease that starts with mucosal inflammation of the rectum and extends proximally in the colon in a continuous manner over a variable distance. Although it is more common in North America and Western Europe, its incidence is also increasing in Asia. Despite the introduction of several different classes of medications, the treatment options for UC may be insufficiently effective and burdened with significant side effects. In the present study, the therapeutic effects of Gancao Xiexin decoction (GCXX) were investigated on mice with dextran sulfate sodium (DSS)-induced colitis with exploration of the underlying mechanisms. Methods Colitis was induced in C57BL/6 mice by administering 3% DSS in drinking water for 7 days. GCXX and (or) the standard of care anti-inflammatory drug, mesalazine (5-aminosalicylic acid) were then administered for 7 days. The gut microbiota was characterized by 16S rDNA high-throughput gene sequencing and gut metabolites were detected by untargeted metabolomics. Germ-free mice were subsequently used to determine whether GCXX ameliorated UC principally through modulation of the gut microbiota. Results GCXX treatment was demonstrated to significantly reduce disease activity index (DAI) scores, prevent colonic shortening, ameliorate colonic tissue damage and reduce the levels of pro-inflammatory cytokines. Furthermore, analysis of the gut microbiota showed that GCXX-treated mice had higher relative quantity of Dubosiella (P<0.05) and lower relative quantity of Escherichia-Shigella (P<0.05). Metabolomics analysis indicated that GCXX could reduce the level of linoleic acid (P<0.05) and regulate its metabolism pathway. Moreover, in germ-free mice, GCXX failed to increase body weight, reduce DAI scores, or alleviate either colonic shortening or colonic damage. Conclusion The present study demonstrated that GCXX ameliorated DSS-induced colitis principally through modulating the gut microbiota and metabolites. This information should be integrated into the overall mechanisms of GCXX treatment of UC.

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Gut dysbiosis and clinical phases of pancolitis in patients with ulcerative colitis

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 18 publications

References 76 publications

The Communication Between Intestinal Microbiota and Ulcerative Colitis: An Exploration of Pathogenesis, Animal Models, and Potential Therapeutic Strategies

The Communication Between Intestinal Microbiota and Ulcerative Colitis: An Exploration of Pathogenesis, Animal Models, and Potential Therapeutic Strategies

Saccharina japonica Ethanol Extract Ameliorates Dextran Sulfate Sodium-Induced Colitis via Reshaping Intestinal Microenvironment and Alleviating Inflammatory Response

Gancao Xiexin Decoction Ameliorates Ulcerative Colitis in Mice via Modulating Gut Microbiota and Metabolites

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