New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease

Liang, Bing; Wu, Changhao; Wang, Chao; Sun, Wenshe; Chen, Wujun; Liu, Ning; Xing, Dongming

doi:10.3389/fmicb.2022.1065608

Cited by 6 publications

(2 citation statements)

References 107 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The presence of adenosine diphosphate, abundant in injured colonic tissue, has been found to activate the NLRP3 inflammasome by regulating P2Y1 receptor-mediated calcium signaling. This activation leads to the maturation and secretion of IL-1β, further exacerbating the progression of colitis [ 95 , 96 , 97 ].…”

Section: Ibd Nlrp3 Inflammasome and Implications Of Plant-derived Int...mentioning

confidence: 99%

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

et al. 2023

View full text Add to dashboard Cite

Ongoing research explores the underlying causes of ulcerative colitis and Crohn’s disease. Many experts suggest that dysbiosis in the gut microbiota and genetic, immunological, and environmental factors play significant roles. The term “microbiota” pertains to the collective community of microorganisms, including bacteria, viruses, and fungi, that reside within the gastrointestinal tract, with a particular emphasis on the colon. When there is an imbalance or disruption in the composition of the gut microbiota, it is referred to as dysbiosis. Dysbiosis can trigger inflammation in the intestinal cells and disrupt the innate immune system, leading to oxidative stress, redox signaling, electrophilic stress, and inflammation. The Nod-like Receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome, a key regulator found in immunological and epithelial cells, is crucial in inducing inflammatory diseases, promoting immune responses to the gut microbiota, and regulating the integrity of the intestinal epithelium. Its downstream effectors include caspase-1 and interleukin (IL)-1β. The present study investigated the therapeutic potential of 13 medicinal plants, such as Litsea cubeba, Artemisia anomala, Piper nigrum, Morus macroura, and Agrimonia pilosa, and 29 phytocompounds such as artemisitene, morroniside, protopine, ferulic acid, quercetin, picroside II, and hydroxytyrosol on in vitro and in vivo models of inflammatory bowel diseases (IBD), with a focus on their effects on the NLRP3 inflammasome. The observed effects of these treatments included reductions in IL-1β, tumor necrosis factor-alpha, IL-6, interferon-gamma, and caspase levels, and increased expression of antioxidant enzymes, IL-4, and IL-10, as well as regulation of gut microbiota. These effects could potentially provide substantial advantages in treating IBD with few or no adverse effects as caused by synthetic anti-inflammatory and immunomodulated drugs. However, additional research is necessary to validate these findings clinically and to develop effective treatments that can benefit individuals who suffer from these diseases.

show abstract

Section: Ibd Nlrp3 Inflammasome and Implications Of Plant-derived Int...mentioning

confidence: 99%

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

et al. 2023

View full text Add to dashboard Cite

show abstract

“…Interventions targeting key regulatory molecules of mucosal immune responses and suppressing or enhancing specific immune pathways or signaling molecules can precisely modulate the activity of the immune system [92]. In mucosal immune responses, prominent proinflammatory cytokines and growth factors include IL-1β, interferon-gamma, TNF-alpha (TNF-α), and IL-6.…”

Section: Treatment Progress Of Autoimmune Diseases Based On Intestina...mentioning

confidence: 99%

Intestinal Mucosal Immunity Caused Autoimmune Diseases

Nie,

Zhang,

Yang

et al. 2023

Probing Selected Autoimmune Diseases for Focused Perspectives

View full text Add to dashboard Cite

Autoimmune diseases are a group of chronic inflammatory disorders caused by the imbalance of immune homeostasis and abnormal production of autoantibodies. The etiology of autoimmune diseases involves various factors such as genetic and environmental factors, and the exact pathogenesis remains unclear. The intestinal mucosal immunity including the intestinal epithelial barrier, mucosal immune cells, and innate immune cells cooperatively maintains intestinal immunity against invading pathogens. It has been demonstrated that intestinal mucosal immunity participates in the development of various autoimmune diseases. Dysbiosis of gut microbiota and their metabolite alterations and immune response mediated by intestinal immune cells may be involved in the pathogenesis of systemic lupus erythematosus through multiple mechanisms. When the intestinal mucosal epithelium is damaged, intestinal flora can penetrate the barriers and enter the lamina propria, causing abnormal immune response and inducing the development of Inflammatory Bowel Diseases. Targeting the gut mucosal immune system holds promise for treating autoimmune diseases; therefore, it is necessary to review the role of the gut mucosal immune system in autoimmune diseases and provide guidance for the treatment of autoimmune diseases.

show abstract

Novel targets for mucosal healing in inflammatory bowel disease therapy

Mansouri,

Behmard

et al. 2025

International Immunopharmacology

View full text Add to dashboard Cite

New insights into bacterial mechanisms and potential intestinal epithelial cell therapeutic targets of inflammatory bowel disease

Cited by 6 publications

References 107 publications

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

Medicinal Plants, Phytochemicals and Regulation of the NLRP3 Inflammasome in Inflammatory Bowel Diseases: A Comprehensive Review

Intestinal Mucosal Immunity Caused Autoimmune Diseases

Novel targets for mucosal healing in inflammatory bowel disease therapy

Contact Info

Product

Resources

About