Wilmore et al. have referred to the intestine as one of the central organs of the stress response in surgical patients. Recent studies have shown that the intestine is the largest peripheral immune organ in the human body, and T lymphocytes and plasma cells in the mesenchyme of the intestinal mucosa produce large amounts of secretory S-IgA under the stimulation of antigen, and this local immune response constitutes the first line of defense of the intestinal mucosal barrier. This is the second line of defense of the immune barrier. When the immune system is compromised, invading bacteria and endotoxins enter the circulation and tissues. Clinical studies have also shown that in trauma, surgery, starvation, and long-term total parenteral nutrition (TPN), the intestinal mucosal barrier is weakened and the permeability of the intestinal mucosa is increased, leading to bacterial translocation, endotoxemia, and even sepsis, with the ultimate result being intestinal failure and life-threatening multi-organ failure. Therefore, it is of great clinical significance to understand the relationship between enteral nutrition (EN) and intestinal barrier function. The normal human intestinal mucosal barrier is composed of intestinal mucosal epithelium, normal intestinal flora, intestinal endocrine and intestine-related immune cells, and a large number of anaerobic bacteria grow on the surface of the intestinal mucosa under normal conditions. In recent years, foreign scholars have also discovered that there exists a kind of M-cells in the intestine, which are the only permeable epithelial cells in the intestinal wall, and antigens, bacteria and viruses can invade the body through this weak link. The maintenance of normal intestinal barrier function depends on specific secretory immunoglobulin S-IgA produced by gastrointestinal-associated lymphoid tissues, as well as non-specific mechanical and chemical barriers such as gastric acid, peristalsis, intestinal epithelial tight junctions, mucus, digestive enzymes, and normal flora. Maintenance of normal epithelium prevents transepithelial bacterial translocation, and protection of tight junctions prevents translocation of bacteria via paracellular channels. The intestinal mucosa has about 5 million villi with a total area of about 10 m2 and in some cases is a dangerous channel for bacteria and toxins to invade the body. When the stress response of the body is excessive or dysregulated, the integrity of the intestinal mucosal barrier can be damaged first, and the permeability of the intestinal mucosa can be increased, so that bacteria and endotoxins previously parasitized in the intestine can cross the damaged intestinal mucosa and invade a large number of tissues outside the intestine, which are normally sterile, such as mucosal tissue, intestinal wall, mesenteric lymph nodes, portal vein and other distant organs and systems, and bacteria (endotoxins) can The bacteria and endotoxin that enter the blood circulation in turn act on the intestinal mucosa, further aggravating the damage of the intestinal mucosal barrier and leading to the continued increase of intestinal mucosal permeability, thus forming a vicious circle, and even the occurrence of systemic inflammatory response syndrome (SIRS) and multi-organ system failure (MOSF). 2. Causes of intestinal mucosal barrier damage 2.1 Increased intestinal mucosal permeability Intestinal mucosal permeability refers to the property that the intestinal mucosal epithelium is easily passed by certain molecular substances in a simple diffusion manner. Clinically, intestinal mucosal permeability mainly refers to the penetration of molecular substances with molecular weight >150 into the intestinal epithelium. Severe infections, trauma, massive burns, and acute pancreatitis can lead to damage of the intestinal mucosal barrier. Increased intestinal mucosal permeability has occurred long before significant changes in intestinal mucosal morphology, so increased intestinal mucosal permeability can reflect early damage to the intestinal mucosal barrier. It is currently believed that a variety of cytokines (cytokines) can cause increased intestinal mucosal permeability, including endotoxin, tumor necrosis factor (TNF), gamma-interferon, interleukin-1 (IL-1), interleukin-2 (IL-2), platelet-activating factor (PAF), and nitric oxide (NO). Endotoxins can cause pathological changes in the ultrastructure of intestinal mucosal epithelial cells and disrupt tight intercellular junctions by damaging the intracellular scaffolding system, resulting in increased intestinal mucosal permeability. TNF increases intestinal epithelial permeability probably through the mechanism of disrupting intercellular tight junctions. However, in vitro studies found that γ-interferon increased the permeability of isolated cultured thin intestinal epithelium to mannitol, while TNF, IL-1 and IL-2 failed to increase the permeability of intestinal epithelium to mannitol at this time. When PAF was administered to mice, it caused significant pathological damage to the gastrointestinal mucosa, resulting in increased absorption of 125I-labeled albumin and 51Cr-EDTA into the blood in their intestinal lumen, possibly through altered intestinal mucosal permeability by activating adherent leukocytes to release oxygen radicals and damage cellular bypass channels. TNF may play a central role in the complex chain reaction of cytokines. It has been shown that endotoxin opens intracellular signaling pathways through the sensitization system of lipopolysaccharide binding protein (LBP) and lipopolysaccharide receptor CD14, stimulates the expression of genes such as tumor necrosis factor (TNF), interleukin-1 (IL-1) and interleukin-6 (IL-6), mediates the activation of monocytes-macrophages, disrupts the balance of pro- and anti-inflammatory factors, and triggers 2.2 Decreased intestinal mucosal support The intestinal mucosal support system consists of a biological barrier composed of normal flora and a robust immune system. Damage to either of these components can lead to overall damage to the intestinal mucosal support system and reduce the ability of mucosal renewal and repair. Long-term fasting or long-term parenteral nutrition can cause the intestinal tract to remain dormant without load for a long time, and the lack of food and digestive tract hormone stimulation in the mucosa can cause intestinal villus atrophy, thinning of the intestinal mucosa, and reduce the ability of mucosal renewal and repair; at the same time, gastric acid, bile, lysozyme, mucopolysaccharide and proteolytic enzymes secretion is reduced, and intestinal fluid In addition, the widespread use of broad-spectrum antibiotics causes dysbiosis of the intestinal flora, which is normally dominated by specialized anaerobic bacteria, and disrupts the intestinal biological barrier composed of normal flora. When the intestinal permeability is increased, bacteria and endotoxins can enter the blood and lymph through the tightly connected gap at the top of adjacent epithelial cells, leading to systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS), and the bacteria and endotoxins that enter the blood circulation in turn act on the intestinal mucosa, further aggravating the intestinal The bacteria and endotoxin in the blood circulation will in turn act on the intestinal mucosa, further aggravating the intestinal mucosa damage until intestinal failure. 3. enteral nutrition on the maintenance of intestinal mucosal barrier 3.1 re-understanding the importance of enteral nutrition When total gastrointestinal nutrition (TPN) was first used in clinical practice, physicians were very enthusiastic to accept this new therapy. tPN was widely used in clinical practice and played a significant role, occupying a major position in clinical nutrition. With more experience in clinical practice and more research, the shortcomings of TPN gradually emerged. Although long-term application of TPN can make patients’ intestines rest and facilitate rapid recovery of nitrogen balance, there are still many problems, the most important of which is still metabolic disorders, such as excessive increase of fat and water, insufficient increase of fat-free meat, intestinal mucosa atrophy and biliary stasis, so enteral nutrition has been given renewed attention. It was also found that during long-term application of TPN, the DNA content of intestinal epithelial cells decreased, protein synthesis was weakened, the thickness of the mucus layer in the intestinal lumen became thinner, the secretion of intestinal SIgA decreased, the number of lymphocytes in the lamina propria of the intestinal mucosa also decreased, and a series of pathophysiological changes occurred in the function of the intestinal mucosal barrier, leading to atrophy and increased permeability of the intestinal mucosa, but after timely application of EN, this situation could be rapidly changed, with the possible The possible mechanism is that some nutrients, such as glutamine can directly provide nutrition to intestinal epithelial cells, long-chain fatty acids provide energy source for small intestine, and short-chain fatty acids provide energy for colon after decomposition into acetate, propionate and butyrate in colon, while intraluminal nutrients can cause the release of various gastrointestinal hormones, stimulate intestinal peristalsis, promote the proliferation of intestinal mucosal epithelial cells and secretion of S-IgA by intestinal endocrine cells and other immunoglobulins. Especially since the mid-1980s, infections caused by intestinal bacterial translocation have become the focus of attention in the field of surgery, and it was found that long-term application of TPN could lead to intestinal mucosal atrophy, intestinal mucosal barrier dysfunction or damage, followed by bacterial translocation. Therefore, in recent years, the importance of enteral nutrition has been re-recognized at home and abroad, especially the research on the protective effect of enteral nutrition on the intestinal barrier. Enteral nutrition helps maintain the integrity of intestinal mucosal cell structure and function, supports the intestinal mucosal barrier, and significantly reduces the occurrence of enteric-derived infections. Especially when the condition is critical, the immunity of the body is reduced, and the low blood flow state of the intestine leads to nutritional damage to the intestinal mucosa, while the metabolism is impaired in the critical state, TPN tends to deviate the metabolism from the physiological process, and the metabolic complications increase, at this time, enteral nutrition is particularly important. At present, people have regained to recognize the importance of enteral nutrition, and it is clearly proposed that enteral nutrition is preferred under the condition that the intestinal function allows. 3.2 Mechanism of enteral nutrition to maintain the intestinal mucosal barrier Recent studies have shown that the mechanism of enteral nutrition to maintain the intestinal mucosal barrier includes: (1) maintaining the normal structure of intestinal mucosal cells, intercellular connections and villi height, maintaining the mechanical barrier of intestinal mucosa; (2) maintaining the normal growth of intestinal intrinsic bacteria ratio, maintaining the biological barrier of intestinal mucosa; (3) contributing to the normal secretion of SIg -A, maintaining the immune barrier of intestinal mucosa; (4) stimulating the secretion of gastric acid and pepsin, maintaining the chemical barrier of mucosa; (5) stimulating the secretion of digestive juices and gastrointestinal hormones, promoting gallbladder contraction and gastrointestinal peristalsis, increasing visceral blood, making the metabolism more in line with the physiological process, and reducing the occurrence of liver and biliary complications. 4.Problems and prospects At present, we have clarified that intestinal mucosal barrier dysfunction, intestinal bacteria and endotoxin migration is an important factor leading to systemic inflammatory response syndrome (SIRS), multi-organ dysfunction syndrome (MODS) and even multi-system organ failure (MSOF), and in terms of prevention, in addition to the application of effective antibiotics, the status of EN is becoming more and more obvious. Therefore, how to apply EN early and when to apply EN; the study of nutritional drugs to maintain the function of intestinal barrier; more reasonable formulation and infusion route of EN will be our key research content in the future.