Correction: The current consensus on ulcerative colitis, and the evidence and perspectives on the influence of gut microbiota on it

stool meaning frequent but poor defecation [6]. There are also some patients with abdominal pain, mostly located in the left lower abdomen dull pain, or intermittent abdominal cramps, with the characteristics of relief after the stool, more serious patients with abdominal pain symptoms, and the increase of the lesion intestinal wall tension related. In addition, UC patients are accompanied by many extra-gastrointestinal symptoms, such as joint complications, peripheral arthropathy and axial arthropathy [7]. The skin showed erythema nodosum, pyoderma gangrenosum and nonspecific rash. Ocular manifestations were scleritis and uveitis.Nonspecific fatty liver, cholelithiasis and primary sclerosing cholangitis [5].Clinical observation of a large number of UC patients, it was found that the initial lesion of the intestinal tissue of patients with UC was manifested as the infiltration of neutral multinucleated cells and round cells in the basement crypt of the mucosa, resulting in crypt abscess [8]. The swelling of mitochondria, the dilatation of intercellular space and the dilatation of inner plasma can be seen clearly in electron microscope [9]. As the disease progresses, the crypt abscess and covering epithelium become detached, leading to ulcers. The ulcer is adjacent to a relatively normal mucosa, but the mucosa is edema, which gives it a polypoid appearance and is isolated between adjacent ulcers. The ulceration area is occupied by the indulgent growth of granulation and collagen tissue, and the ulceration is aggravated, but penetration of the musculature is less common. In toxic megacolon and explosive UC such lesions may penetrate the entire intestinal tissue and present as intestinal perforation, but these lesions are rare. The patient has about 20 bloody stoes every day.Due to the light peeling of the intestinal wall and the obviously deformed mucous membrane cannot effectively absorb water and sodium, every peristalsis will squeeze out a large amount of blood from the exposed granulation tissue surface, so the mucosal abscess and blood of this disease is more obvious than that of Rohn's disease [10; 11; 12].UC, as a recurrent and refractory digestive disease, is closely associated with colorectal cancer, but the exact etiology has not yet been determined [13]. UC is greater customary in developed international locations than in growing countries, however the incidence in creating nations is getting greater and higher. The gut microbiota, mucosal barrier damage, and immune response regulation are affected by nutritional imbalance and dietary factors [14].Environmental health, lifestyle and other factors will also increase the risk of UC.Studies consistently show that smoking has an important impact on the incidence of UC [15]. Compared with non-smoking, smokers have a greatly increased risk of UC, and smoking patients are usually more serious [16; 17]. Studies have shown that eating vegetables and fruits can greatly reduce the risk of UC [18]. On the contrary, meat consumers have a significantly increased risk of UC than vegetarian consumers, and the relationship between red meat and UC is more significant among meat consumers.In addition, drinking a large number of beverages will also increase the risk of UC [19]. Alcohol can directly cause mucosal damage and increase bacterial migration, which is a risk factor for UC [20]. The amount of n-3polyunsaturated fatty acids (n-3 PUFAs) in the diet is negatively correlated with UC. The more unsaturated fatty acids (n-3 PUFAs) are consumed, the lower the risk of UC. In order to maintain health, human essential fatty acids OMEGA 3 (a linoleic acid) and OMEGA 6 (oleoleic acids) are necessary, the body can not manufacture, must be obtained from the exogenous diet, but too much intake of OMEGA 3 and OMEGA 6 will increase the risk of UC [21]. However, caffeine can delay the mice colitis induced by sodium glucan sulfate by down-regulating chitosinase 3-like protein 1 [22]. In addition, tea is rich in tea polyphenols, which have significant effects on anti-inflammatory and antioxidant aspects, so drinking tea can reduce the risk of UC [23; 24]. Gastrointestinal infections can also double the risk of UC. Salmonella, Shigella, and Campylobacter motive adjustments in the intestine microbiota, which can additionally be considered in the use of antibiotics to deal with these prerequisites [25; 26].It is estimated that 11.6 out of every 100,000 Chinese suffer from UC, according to a large number of statistical studies, especially in the southeastern coastal areas with Westernized lifestyles, North America and Europe have higher rates of UC than Asia, with 156 to 291 cases per 100,000 people [27]. With the foremost onset height between the a while of 15 and 30 and between the a long time of 50 and 70, but there appears to be no specific gender preference [26; 28]. In addition, IBDoften appears with hereditary familial characteristics. Modern gene detection techniques have found multiple IBD susceptible regions (such as 1p36, 21q22) and susceptible genes (such as TNFSF15, IL-23R, and IL-12B), and the multi-gene single nucleotide polymorphisms in susceptible regions suggest that they may be related to inflammation [29]. The closest relationship with UC is HLA-Ⅱ genes, in which DR2 and DR9 at the DR Site are considered to be susceptible genes to UC, whereas DR4 is a defensive gene and promotes the expression stage of HLA-DR antigen in the colon mucosal epithelium of UC sufferers [29; 30].Researchers have found that UC results in a balance to be upset between the antigen-presenting cells, the helper T cells, the regulatory T cells, and the natural killer T cells. As a result, pro-inflammatory cytokines are up-regulated and anti-inflammatory cytokines are down-regulated, which are key factors in the damage to the UC mucosa [31; 32]. The production of interleukin-13 has cytotoxic effects on epithelial cells, as it induces apoptosis and alters the composition of tight junction proteins [33]. Tumor necrosis factor (TNF) levels increase in patients with UC' blood, stool samples, and mucosa [34]. There is a clear link between Tumour Necrosis Factor-a (TNF-a) and UC, which confirms that TNF-a plays a significant role in its development [35; 36]. Neutrophils, as the effect cells of innate immunity, are active cells to defend against pathogen invasion. However, the unregulated mechanism of neutrophils inflammation will accelerate tissue damage and further destroy the balance of the intestinal environment. Abnormal neutrophils function can be used as early screening for chronic intestinal inflammation, and can also reflect adaptive immune function.Neutrophil infiltration in the intestinal mucosa is a key aspect of UC's pathophysiology, with the severity of the disease being closely linked to both the degree and timing of neutrophil migration. Activated neutrophils migrate to the site of inflammation through the epithelial space and accumulate in the crypt cavity to cause crypt abscess, which is the characteristic histological and pathological change of UC [37]. Among the intestinal microbiota, the colon is the primary settlement site since it offers rich nutritional conditions to the microbiota [38]. Intestinal microbiota imbalance has been shown to play a significant role in UC pathogenesis more and more studies are showing. It is bacterial growth in the human digestive tract that plays a role in the formation of mucosal barriers and maintains the stability of the intestinal environment, as well as protecting the intestinal submucosa, it triggers immune response by protecting it from gut microbiota and various toxins [39]. Through metabolic products, microorganisms in the intestinal tract provide energy and nutrients to the host and regulate their immune function [40; 41]. Known as probiotics, they are live, nonpathogenic bacteria, including Lactobacillus, Bifidobacterium, and Enterococcus. Bacteria in probiotics promote gut and immune health by restoring mucosal barrier function that has been damaged, optimizing intestinal barrier function, improving gut microbiota balance, inhibiting pathogen competition, and improving immunity locally and systemically [42]. It is known that probiotics secrete the most short-chain fatty acids, actic acid, butyric acid, and propionic acid. Butyrate promotes the intestinal immune system, protects intestinal epithelium integrity, inhibits tumor cell growth, and provides many other health benefits, and reduces cancer-promoting enzyme activity in the body, thereby reducing intestinal inflammation and colorectal cancer by protecting the intestinal wall [43].Lactobacillus and bifidobacterium in Firmicutes and actinomyces of probiotics can synthesize vitamins and other substances needed by the human body, inhibits the growth of pathogenic bacteria as well. In the gut microbiota of patients with active UC, bifidobacterium and lactobacillus levels were significantly reduced, as well as the abundance of gut microbes [44]. On the contrary, harmful bacteria such as salmonella, clostridium difficile, Clostridium perfringens and other large numbers of growth and reproduction, will cause a variety of diseases, and even produce carcinogens, if UC patients infected, will aggravate the progression of the disease and the evolution of cancer [45]. Opportunistic pathogens are beneficial to human health in normal quantities, but once their proliferation is out of control or gut microbiota shifts occur, diseases such as sepsis and septic shock will occur. For example, Escherichia coli in Proteobacteria, as a normal resident bacterium in human body, can not only inhibit the growth of some intestinal microorganisms, but also reduce the harm of protein decomposition products to human body. 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