The intestinal herb and gastrointestinal health: the mystery you don’t know.

In our body, there’s a huge and mysterious microworld, a intestinal herb. The intestinal fungus interacts with the gastrointestinal mucous barrier, which together affects our health. Today, we come to unmask their mysterious veils and see how the intestinal fungus regulates the gastrointestinal mucous barrier, thus affecting our health. The intestinal barrier: the fine design of the structure and function of a healthy guardian, our gastrointestinal tract is like a strong castle, and the intestinal barrier is the guardian of this castle. From the oesophagus to the big intestines, the entire digestive tract is covered with mucous membranes, forming a natural line of defence. The line consists of a biological barrier, a chemical barrier, a mechanical barrier and an immune barrier, which work together to protect against the invasion of external pathogens. The intestinal population: the main force of the biological barrier The intestinal population is an important component of the biological barrier, as are the soldiers in the castle, who are numerous and do their job. Bacteria in the human intestinal tract are alarming, at 1013-1014 CFUs of up to 400-500 species. The bacteria are planted in the intestinal tract and symbiotic with the host. They prevent the planting and growth of harmful strains by competing for nutrients and by taking a place on the surface of the intestinal mucous membranes, thereby protecting the intestinal tract from pathogens. The mucous shield that protects the intestine, which is an important part of the intestinal barrier, is like a soft, tenacity shield that protects the intestinal skin cells. The mucous layer of the intestines is a loose, unilayered structure, while the mucous layer of the colon is divided into two layers, with the inner layer closely attached to the intestine cell and the outer layer relatively loose, providing nutrients and coding points for the intestinal population. The mucous layer consists mainly of mucous protein MUC2, which not only prevents the interaction of pathogens with host cells, but also maintains a community balance. The changes in the fungus of the MUC2 defective mice, leading to mild colonitis, indicate that MUC2 plays a vital role in maintaining intestinal health. The intestinal skin cells: the closely connected dæmonies, the intestinal skin cells form a tight line of defence by closely linking proteins to prevent the passage of harmful substances. These closely connected proteins are like members of the Guardian Alliance, working closely to regulate intestinal penetration. When the close connection is damaged, the intestinal barrier is impaired, leading to pathogens and harmful substances entering the body, causing inflammation and disease. intestinal immunisation barriers: immune cells on the defensive front of immunosuppressive cells The immune cells in the inner intestinal layers form intestinal immune barriers, they are always alert to the invasion of pathogens and, if abnormalities are detected, the immune response is activated quickly. The intestinal skin cells isolate the intestinal fungus and host immunocellular cells through physical and chemical barriers to avoid overimmunisation and maintain symbiotic relationships. The intestinal fungus also regulates the host ‘ s immune defence and resistance through metabolites and pathogenic bacterial components, promoting the maturity of congenital and adaptive immune functions and maintaining intestinal stability. The close interaction of intestinal strains with the intestinal mucous barrier: the strong assistant of the mucous barrier The intestinal fungus plays an important role in the intestinal barrier function. They can spread mucous factors, metabolites, etc., and participate in the construction of chemical barriers; activate immunocells to produce antibodies and cytogens to enhance the functioning of the immune barrier; and promote close intercellular connections and mucous membranes and maintain the integrity of the mechanical barrier. For example, Mincle identifies mucous microbial symbiotics, triggers lymphoctology IL – 6, IL – 23, maintains the intestinal mucous barrier and limits bacterial transfer and hepatitis. The intestinal morbidity: the curator behind the intestinal mucous lesion, however, becomes the curator of the intestinal mucous lesion when the intestinal figment. Genetic susceptibility, fungi, environmental factors (e.g., fat diets, drugs/antibiotics) can all lead to intestinal group disorders. The intestinal tumour disorders can damage the upper intestinal cortex, causing inflammatory diseases (e.g. ulcer ulcer, cronosis, lactation), metabolic diseases (e.g. obesity, diabetes) and systemic diseases/outside manifestations, which can also lead to immunological abnormalities, changes in bacterial metabolites and metabolic internal toxin haemorrhage. Controlling intestinal strains: The magic effect of a new strategy to maintain intestinal barriers is that of a type of micro-organisms that are beneficial to the host and that can maintain intestinal barriers in many ways. For example, the fungi/butyric acid gastrics can effectively reduce the mucous membrane penetration of DSS mice and restore intestinal stability; the fessy intestinal fungus R-026 can effectively restore closely connected protein expression to the upper intestinal skin, and prevent DSS induced intestinal mucous membrane damage; and the dead Bacillus R-179 can restore the intestinal mucous barrier of the AOM/DSS induction mouse model and promote closely connected protein expression to the upper intestinal skin. In addition, prophylactic molecules can combine with model recognition receptors, regulate intestinal inflammation and immune factors and maintain intestinal barriers. The synergy between the living and congener is a substance that cannot be absorbed by humans, but can be used in the intestines for the benefit of fungi, which promotes the growth and reproduction of beneficial bacteria. The symbiotic symbiology is a combination of the fungi and the symbiotic symbiotic symbiosis, which can work in synergy and better regulate the intestinal herbs. Studies have shown that complementary living dollars (e.g., lactating nuts) can improve the intestinal barrier function of DSS for mice, increasing the levels of mucous membrane barrier proteins such as Occludin, E-Cadherin and ZO-1. Butate: The repair master of the intestinal barrier Butate is one of the important metabolic products of the intestinal fungus, which has an important regulatory effect on the intestinal barrier function. Normal concentrations of butate increase the MUC2 expression, irritating mucous protein production and genocination, thereby enhancing the intestinal barrier function. However, high concentrations of butate may inhibit MUC2 expression, which is associated with the collapse of high concentrations of butate-inducing cells. Pioneer fungus: The key force for re-establishing intestinal microecologicals is especially critical when intestinal strains are disturbed. The bacterium bacterium is a pre-emptive fungus with multiple mechanisms of action. Bacillus is a good fungus, capable of rapidly depleting oxygen, reducing intestinal oxygen fraction pressure and restoring anaerobic conditions in the intestinal environment; butic acid is metabolismed in the faeces, which restore normal performance of intestinal skin cells; and co-opt oxygen, re-establishing normal aerobic conditions in the intestinal tract, increasing the number of beneficial bacteria, reducing the number of harmful bacteria, balancing intestinal strains, repairing the intestinal mucous barrier and maintaining its integrity. The mythological association of intestinal bacteria with chronic diseases (IBD): The intestinal strain structure of IBD patients with intestinal inflammation caused by intestinal inflammation has changed, the diversity has decreased, the fungus and thick flask doors have decreased, and there has been an increase in nematodes and deformation, especially in intestinal bacteria (a visceral invasive coliform bacteria). At the same time, UC patients suffered from a decrease in anaerobic butic acids, damage to intestinal barriers, and inflammation caused by intestinal strains through immunotransmission. Non-alcoholic fatty liver disease (NAFLD): The chain reaction of micro-ecological imbalances The intestinal micro-ecological imbalances play an important role in the development of NAFLD. The intestinal strain causes increased intestinal barrier penetration, bacterial transposition and metabolic logistics to the liver, which triggers and exacerbates NAFLD. Its mechanisms include changing the ability to absorb energy in the diet, influencing fat generation and short-chain fatty acid synthesis pathways, changing choline and cholesterol metabolic signal circuits, increasing intestinal penetration and inflammation, and generating internal alcohol in the intestinal tract. Sphinocella (Hp) infection: The double effects of gastrointestinal and intestinal strains. Hp Decreased abundance and diversity of intestinal fungus in patients with stomach inflammation and also led to intestinal fungi disorders. After the Hp eradication treatment, the intestinal deformation door increased, and the coil/wielding door decreased. The intestinal strain is one of the main causes of Hp’s adverse effects on eradication. Summarizing and looking at the relationship between intestinal bacteria and gastrointestinal mucous barriers is like a wonderful dance that interacts, interacts, and together sustains the health of the intestinal tract. When intestinal strains occur, the intestinal barrier is impaired, leading to various diseases. By regulating intestinal strains, we can maintain intestinal barriers and prevent and treat related diseases. In future research, we need to further deepen our understanding of the mechanisms for interaction between intestinal strains and gastrointestinal mucus barriers, and explore more effective methods of regulation to provide better protection of intestinal health. At the same time, care should be taken to maintain a healthy lifestyle, such as a reasonable diet, adequate exercise, reduced use of antibiotics, etc., in order to maintain a balance in the intestinal population and to protect our intestinal health.