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Intestinal microbes are taxonomically diverse and constitute an ecologically dynamic microbiom interactively performing various physiological and physiopathological processes. It has been proposed that normal intestinal microbiotas play a critical role in the host’s metabolic homeostasis and immune tolerance. The modulation of intestinal microbiota populations by prebiotics, probiotics, and synbiotics may be beneficial for the host’s health. Under certain conditions, the intestinal microbiota and the host’s homeostasis can be restored by introducing bacteria that co-mediate anti-inflammatory responses. Commensal microbes and probiotics exert their beneficial effect by at least three mechanisms. These include – the maintenance of the epithelial barrier function and the attenuation of changes in intestinal permeability through effects on tight junction, decreasing paracellular permeability, providing innate defense against pathogens, and enhancing the physical impediment of the mucous layer, – competitive exclusion by the application of probiotic bacteria stabilizing the indigenous microflora, – immunomodulatory capacity, affecting a variety of signaling pathways with modulation of proper immune, inflammatory and allergic responses. The epithelial gut barrier faces important challenges, since its function is to prevent pathogens and harmful elements of the gut lumen from penetrating into the internal environment. Competitive exclusion treatment can increase resistance to pathogen colonization and control intestinal disturbance. The dominance of symbiotic and probiotic bacteria among the gut microbiota favors a tolerogenic immune response. The release of secretory IgA stabilizes tight junctions between cells of the epithelial layer as well as hampers pathogens and symbionts invading deeper layers. The understanding of these vital processes may help to protect the host against infection, prevent chronic inflammation, and maintain mucosal integrity.
The gastrointestinal tract in humans and animals contains a very large number of highly diverse microorganisms. This microbiota plays a major role in the host’s physiology, homeostasis, and well-being. It forms a barrier against infection, helps to develop and mature the immune system, and participates in the extraction of nutrients and energy from food. Various members of microbial community maintain the integrity of the intestinal barrier and promote epithelial repair after injury. The intestinal barrier defenses consist of the mucous layer, antimicrobial peptides, secretory IgA, and the epithelial barrier function by junctional adhesion complex. A healthy host exists in a state of balance with its microorganisms. A disruption of the microbial community increases the host’s susceptibility to infection. Although the immune response is necessary for the host to eliminate the invading pathogen, certain aspects of the host’s response may work to the pathogen’s advantage. Certain components of the microbiota have been shown to drive inflammatory response, which, if uncontrolled, has the potential to induce a pathological response, whereas others enhance or promote antiinflammatory responses. The effector microbial molecules are usually detected via receptor-signaling pathways including Toll-like receptors, NOD-like receptors, and C-type lectin receptors. These pattern-recognition receptors (PRRs) interact with and identify microbe-associated molecular patterns (MAMPs) of both commensal and pathogenic bacteria. PRRs signaling, once thought to exclusively yield pro-inflammatory activation by pathogenic bacteria, is now known to be differentially activated by commensal and probiotic bacteria to induce pathways involved in gut homeostasis, cytoprotection, epithelial cell proliferation, regulation of tight junctions, and antimicrobial peptide secretion. The microbial-epithelial cross-talk is fundamental in appreciating how the developing intestine achieves tolerance to bacteria and how dysregulation of this process may predispose the gut to inflammation and disease.
Background. The ketogenic diet (KD) has been used for almost 100 years in the treatment of drug-resistant epilepsy in children - and adults. The intestinal microbiome has a climax character, and the main factor changing its composition and functions is the diet. Both increased biodiversity and the production of short-chain fatty acids (SCFAs) are important indicators of gut barrier function. SCFAs are synthesized by microorganisms through the fermentation of dietary fibre provided with the diet. They are an important element in signal transduction from the digestive system to other tissues. To date, there is little research to determine how the use of KD alters the SCFAs profile of the human stool. Objective. To assess the SCFAs profile in the stool of healthy and active KD users. Material and methods. Study group: amateur athletes following KD. Control group: amateur athletes following a regular diet (carbohydrates min. 50%); gender: men and women aged 18-60. Material: stool sample (1x10 g). SCFAs content was determined in stool samples using gas chromtography method. Participants completed a Food Frequency Questionnaire (FFQ) and a 72-hour food diary. Results. There research has shown differences in the amount of SCFAs, as far as the results obtained from the two groups are concerned. The discrepancies referred to the levels of acetic, butyric, iso-butyric, valeric, and isovaleric acids. Spearman's rank correlation analysis showed a strong relationship between the consumption of selected dietary components (vegetables, fruits, red meat, poultry, fish, nuts and seeds, sugar, sugar substitutes, fats) and the SCFAs content in the stool of the study group. Conclusions. High consumption of cruciferous and leaf vegetables, berries and nuts on a ketogenic diet may have a positive effect on the profile of short-chain fatty acids produced by the gut microbiome. Changing the diet towards a greater supply of plant products may prevent proteolytic fermentation and reduce the negative effects of microbiome changes caused by an oversupply of protein and fat in the ketogenic diet.
Chicken ceca contain an immense number of microorganisms collectively known as the microbiome. This community is now recognized as an essential component of the intestinal ecosystem and referred to as a metabolic organ exquisitely tuned to the host’s physiology. These functions include the ability to process otherwise indigestible components of the feed, converting them into energy and body mass. The gut microbiome can also affect intestinal morphology and modulate the development and function of the immune system. This microbiota contains a rich collection of genes encoding enzymes necessary for decomposition of dietary polysaccharides and oligosaccharides, nitrogen metabolism, fatty acid and lipid metabolism, and pathways involved in a hydrogen sink. Chickens, like most animals, lack the genes for glycoside hydrolase, polysaccharide lyase, and carbohydrate esterase enzymes that are necessary to facilitate the degradation of non-starch polysaccharides. During the decomposition of dietary polysaccharides, bacteria produce short-chain (volatile) fatty acids (SCFAs), such as acetic, propionic and butyric acid. These SCFASs are absorbed transepithelially and serve as a source of energy for the host. The accumulation of molecular hydrogen released during fermentation leads to fermentation slowdown or to the production of less energy-efficient substances, such as ethanol, butyrate and propionate. The presence of bacteria that act as a hydrogen sink results in a switch to the more productive fermentation into acetate and increased production of SCFAs. Such activity could lead to a significant improvement in poultry production and the associated economics.
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