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: Colitis is a chronic condition affecting millions worldwide. Purple muscadine wine polyphenols have a unique composition and possible disease-preventive properties. This study aims to determine how dealcoholized muscadine wine (DMW) affects the development of colitis and gut microbiome in IL-10 mice, compared to wild types (WT). : Six-week-old male IL-10 and WT C57BL/6 mice were fed either a DMW-supplemented diet (4.8% /) or a control diet based on AIN-93M for 154 days. Colitis severity was evaluated by disease activity, intestinal permeability, gene expression of cytokines and tight junction proteins in the colon, and inflammatory cytokines in the serum. Fecal samples were collected for gut microbiome profiling via 16S rRNA gene sequencing. : DMW contained predominantly anthocyanins and a significant amount of ellagic acid. IL-10 mice developed mild colitis as indicated by the disease activity index. DMW × gene interactions decreased intestinal permeability, colonic mRNA levels of IL-1β, and serum TNF-α in the IL-10 mice. DMW suppressed the colonic mRNA levels of IL-6, enhanced the gene expression of ZO-1, but did not influence the mRNA level of TNF-α or occludin. While DMW did not alter α-diversity of the gut microbiome, it significantly influenced β-diversity in the WT mice. DMW significantly reduced the relative abundances of in the IL-10 and WT mice. DMW and DMW×gene interaction decreased the relative abundance of only in IL-10 mice. : These results suggested that polyphenols from DMW interacted with genes to moderately alleviate the development of colitis in IL-10 mice and could be a useful dietary strategy for IBD prevention.
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http://dx.doi.org/10.3390/nu17142327 | DOI Listing |
Alzheimers Res Ther
September 2025
Department of Neurology, Saarland University, Kirrberger Straße, 66421, Homburg/Saar, Germany.
Background: Alzheimer's disease (AD) patients and animal models exhibit an altered gut microbiome that is associated with pathological changes in the brain. Intestinal miRNA enters bacteria and regulates bacterial metabolism and proliferation. This study aimed to investigate whether the manipulation of miRNA could alter the gut microbiome and AD pathologies.
View Article and Find Full Text PDFOncogene
September 2025
Department of Molecular Medicine and Biochemistry, Akita University Graduate School of Medicine, Akita, Japan.
Forkhead-box-protein P3 (FOXP3) is a key transcription factor in T regulatory cells (Tregs). However, its expression and significance in non-immune stromal cells in the tumor microenvironment remain unclear. Here, we demonstrated FOXP3 expression in stromal fibroblasts of mouse and human gastrointestinal tumors.
View Article and Find Full Text PDFJ Immunol
September 2025
Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, Qidong-Fudan Innovative Institution of Medical Sciences, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, Shanghai, China.
Hepatitis B virus (HBV) exclusively infects hepatocytes and produces large quantities of subviral particles containing its surface antigen (HBsAg). T cells play a central role in controlling HBV infection but can also mediate liver injury and contribute to disease progression. However, the mechanisms that regulate T-cell responses to eliminate the virus without causing immunopathology during acute HBV infection remain poorly defined.
View Article and Find Full Text PDFProbiotics Antimicrob Proteins
September 2025
Key Laboratory of the Ministry of Education for Wildlife and Plant Resources Conservation in Southwest China, College of Life Sciences, China West Normal University, Nanchong, Sichuan, China.
Enterotoxigenic Escherichia coli (ETEC) is a prevalent intestinal pathogen that significantly impacts both human and animal health. G83, isolated from giant panda feces, has demonstrated notable probiotic properties. In this study, C57BL/6 J mice were randomly divided into Control, ETEC, and G83 groups.
View Article and Find Full Text PDFJCI Insight
September 2025
Arthur D. Riggs Diabetes and Metabolism Research Institute, The Beckman Research Institute, and.
Steroid-refractory gut acute graft-versus-host disease (SR-Gut-aGVHD) is the major cause of nonrelapse death after allogeneic hematopoietic cell transplantation. High numbers of donor-type IL-22+ T cells, IL-22-dependent dysbiosis, and loss of antiinflammatory CX3CR1hi mononuclear phagocytes (MNPs) play critical roles in SR-Gut-aGVHD pathogenesis. CEACAM1 on intestinal epithelial cells (IECs) is proposed to regulate bacterial translocation and subsequent immune responses in the intestine.
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