Inflammatory Bowel Disease (IBD) is a chronic relapsing-remitting disease with a remarkable increase in incidence worldwide and a substantial disease burden. Although the pathophysiology is not fully elucidated yet an aberrant immune reaction against the intestinal microbiota and the gut microbial dysbiosis have been identified to play a major role. The composition of gut microbiota in IBD patients is distinct from that of healthy individuals, with certain organisms predominating over others. Differences in the microbial dysbiosis have been also observed between Crohn Disease (CD) and Ulcerative Colitis (UC). A disruption of the microbiota's balance can lead to inflammation and intestinal damage. Microbiota composition in IBD can be affected both by endogenous (i.e., interaction with the immune system and intestinal epithelial cells) and exogenous (i.e., medications, surgery, diet) factors. The complex interplay between the gut microbiota and IBD is an area of great interest for understanding disease pathogenesis and developing new treatments. The purpose of this review is to summarize the latest evidence on the role of microbiota in IBD pathogenesis and to explore possible future areas of research.
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http://dx.doi.org/10.1016/j.dld.2023.11.015 | DOI Listing |
The gastrointestinal microbiome influences physiological functions and is altered in a variety of diseases. The causality of "dysbiosis" in the pathogenesis is not always proven; association studies are often involved. Patients with IBD, bacteria, fungi, bacteriophages, and archaea show disease-typical patterns associated with metabolome disturbances.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Cardiovascular, Endocrine-Metabolic Diseases and Aging, Istituto Superiore di Sanità, Rome, Italy.
Background: Bacterial toxins are emerging as promising hallmarks of colorectal cancer (CRC) pathogenesis. In particular, Cytotoxic Necrotizing Factor 1 (CNF1) from E. coli deserves special consideration due to the significantly higher prevalence of this toxin gene in CRC patients with respect to healthy subjects, and to the numerous tumor-promoting effects that have been ascribed to the toxin in vitro.
View Article and Find Full Text PDFAnn Rheum Dis
January 2025
Meinig School of Biomedical Engineering, Cornell University, Ithaca, New York, USA. Electronic address:
Objectives: This study aims to elucidate the microbial signatures associated with autoimmune diseases, particularly systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD), compared with colorectal cancer (CRC), to identify unique biomarkers and shared microbial mechanisms that could inform specific treatment protocols.
Methods: We analysed metagenomic datasets from patient cohorts with six autoimmune conditions-SLE, IBD, multiple sclerosis, myasthenia gravis, Graves' disease and ankylosing spondylitis-contrasting these with CRC metagenomes to delineate disease-specific microbial profiles. The study focused on identifying predictive biomarkers from species profiles and functional genes, integrating protein-protein interaction analyses to explore effector-like proteins and their targets in key signalling pathways.
J Agric Food Chem
January 2025
Institute of Food Sciences and Technology, National Taiwan University, Taipei 10617, Taiwan.
Curcuminoids, found in turmeric ( L.), include curcumin (CUR), demethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC). Although CUR and DMC are well-studied, the anti-inflammatory effects of BDMC remain less explored.
View Article and Find Full Text PDFJ Inflamm Res
January 2025
Cancer Center, Daping Hospital, Army Medical University, Chongqing, People's Republic of China.
Inflammatory bowel disease (IBD) is a non-specific inflammatory disease of digestive tract, primarily manifesting as ulcerative colitis (UC) and Crohn's disease (CD). The precise etiology of IBD remains elusive. The interplay of genetic factors, environmental influences, and intestinal microbiota contributes to the establishment of an uncontrolled immune environment within the intestine, which can progressively lead to atypical hyperplasia and ultimately to malignancy over a long period.
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