Inflammatory bowel disease (IBD) belongs to a group of chronic diseases characterised by periods of exacerbation and remission. Despite many studies and observations, its aetiopathogenesis is still not fully understood. The interactions of genetic, immunological, microbiological, and environmental factors can induce disease development and progression, but there is still a lack of information on these mechanisms. One of the components that can increase the risk of occurrence of IBD, as well as disease progression, is oxidative stress. Oxidative stress occurs when there is an imbalance between reactive oxygen species (ROS) and antioxidants. The endogenous and exogenous components that make up the body’s antioxidant defence can significantly affect IBD prophylaxis and reduce the risk of exacerbation by neutralising and removing ROS, as well as influencing the inflammatory state.

Inflammatory bowel disease (IBD) is a group of diseases with a chronic course, characterized by periods of exacerbation and remission. One of the elements that could potentially predispose to IBD is, among others, a low-fiber diet. Dietary fiber has many functions in the human body. One of the most important is its influence on the composition of the intestinal microflora. Intestinal dysbiosis, as well as chronic inflammation that occurs, are hallmarks of IBD. Individual components of dietary fiber, such as β-glucan, pectin, starch, inulin, fructooligosaccharides, or hemicellulose, can significantly affect preventive effects in IBD by modulating the composition of the intestinal microbiota or sealing the intestinal barrier, among other things. The main objective of the review is to provide information on the effects of individual fiber components of the diet on the risk of IBD, including, among other things, altering the composition of the intestinal microbiota.

Inflammatory bowel diseases (IBDs) are a group of chronic diseases characterized by recurring periods of exacerbation and remission. Fibrosis of the intestine is one of the most common complications of IBD. Based on current analyses, it is evident that genetic factors and mechanisms, as well as epigenetic factors, play a role in the induction and progression of intestinal fibrosis in IBD. Key genetic factors and mechanisms that appear to be significant include NOD2, TGF-β, TLRs, Il23R, and ATG16L1. Deoxyribonucleic acid (DNA) methylation, histone modification, and ribonucleic acid (RNA) interference are the primary epigenetic mechanisms. Genetic and epigenetic mechanisms, which seem to be important in the pathophysiology and progression of IBD, may potentially be used in targeted therapy in the future. Therefore, the aim of this study was to gather and discuss selected mechanisms and genetic factors, as well as epigenetic factors.