Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by persistent nonspecific inflammation of the intestine, usually recurrent and prolonged. The exact pathogenesis is unclear, involving immune, environmental and genetic factors that combine to induce inflammation and influence subsequent mucosal damage and repair, and there is still no specific clinical treatment available. There is growing evidence that the gut microbiota is involved in the pathogenesis of IBD. The gut microbiota is essential for the pathogenesis of IBD; the diversity of gut flora in IBD patients differs from that in healthy subjects; the production of metabolites associated with gut microbes is abnormal in IBD patients; some probiotic preparations can modulate the gut flora and alleviate IBD-related symptoms in IBD patients; and some antibiotics and antituberculosis drugs may be effective in the treatment of IBD. This article will focus on the progress of research on the relationship between intestinal microbiota and inflammatory bowel disease. Early studies focused on certain pathogenic bacteria, such as mucosal invasive Escherichia coli and Mycobacterium avium subsp. paratuberculosis in the ileal mucosal epithelium, and found that Salmonella spp., Campylobacter jejuni and Helicobacter pylori infections may increase the risk of IBD occurrence or recurrence. At this stage, more and more scholars have begun to focus on the changes in the overall composition of the intestinal bacterial community, involving differences in the intestinal bacterial community at different sites and states, such as fecal, mucosal, ulcerative site/non-ulcerative site, and remission/acute phase, and have found some characteristic changes. For example, IBD patients had lower levels of intestinal phylum Bacteroidetes and Sclerotinia and higher abundance of Enterobacteriaceae than healthy individuals; CD patients had lower levels of ileal Clostridium perfringens. The metabolites associated with the intestinal bacterial community play an important role in IBD, for example, butyric acid is not only a major source of energy for intestinal epithelial cells, but also prevents signaling of pro-inflammatory cytokine expression. butyric acid-producing bacteria such as Clostridium flexneri and Clostridium spheroides are reduced in the intestine of IBD patients, while the utilization of butyric acid is reduced. Butyric acid-producing bacteria improved intestinal inflammation and necrosis in a rat model, and culture supernatant of butyric acid-producing bacteria improved intestinal inflammation in rats. It has been suggested that the altered intestinal bacterial communities in patients with diarrheal irritable bowel syndrome and UC are similar, showing a reduction in the diversity and abundance of bacterial communities of the intestinal genera Aspergillus oryzae, Aspergillus ovalis, and Aspergillus monomorphicus, as well as the genus Aeromonas. In addition, chronic inflammation of the intestine caused by IBD can increase the risk of colorectal tumors by 5-fold, and IBD colonic lesions can increase the microbial tumorigenic effect. changes in the intestinal bacterial community and metabolites of IBD and colorectal tumors are also similar, showing an increase in the content of intestinal sulfate-reducing bacteria and a decrease in the content of short-chain fatty acid-producing bacterial species. However, the correlation between changes in intestinal bacterial communities and their metabolites in IBD, irritable bowel syndrome and colorectal tumors remains to be further confirmed. The exact type of bacteria or bacterial community composition that contribute to the development of IBD remains unclear, and the causal relationship between altered intestinal bacterial community composition and IBD is inconclusive. Evidence suggests that fungi and their communities are strongly associated with IBD, particularly CD. patients with active IBD have elevated levels of Candida albicans colonization in the stool and at sites of intestinal mucosal inflammation, and clinical symptoms and intestinal inflammation are relieved by antifungal drug therapy. Anti-brewer’s yeast antibody is one of the serological markers of CD. 50% to 60% of CD patients and 20% to 25% of healthy relatives are positive for anti-brewer’s yeast antibody. Studies have confirmed that Candida albicans spp. can induce the body to produce anti-brewery yeast antibodies, and the level of anti-brewery yeast antibodies in healthy relatives of CD patients is consistent with changes in the level of Candida albicans in the gut, but no correlation was found between the level of anti-brewery yeast antibodies in CD patients and the level of Candida albicans in the gut, and it remains controversial whether there is an increase in intestinal Candida albicans in CD patients. In addition, variation in the NOD2 gene reflecting genetic susceptibility to CD was associated with increased anti-brewer’s yeast antibodies. inflammatory mucosa and blood levels of cytokine IL-17 are higher in patients with IBD, and intestinal colonization by Candida albicans increases IL-17 levels in the intestinal mucosa. However, some studies have treated CD with human-derived anti-IL-17A polyclonal antibodies, but the effect was not significant, considering that it may be due to fungal influence. Fungal sequences were detected in the colonic mucosa of IBD patients, but their proportion in the intestinal microbial community was very low. the composition of the fungal community in the intestine of IBD patients changed significantly, with a significant increase in diversity, but whether the changes were secondary to an imbalance in the intestinal bacterial community or an independent pathogenic factor of IBD needs to be further investigated. Imbalance in host immunity to microorganisms or impaired innate and acquired immune function in the intestinal mucosa of IBD hosts has an important impact on the pathogenesis of IBD. Intestinal mucosal epithelial cells are in constant contact with intestinal flora and recognize intestinal bacteria and/or fungi through pathogen recognition receptors such as intracellular NOD-like receptors, extracellular Toll-like receptors, and lectin receptors. In addition, microbial antagonistic substances such as defensins, lectins, and the complement system may also provide continuous bacterial/fungal recognition and defense. The presence of racial differences, family clustering and high co-prevalence with monozygotic twins in IBD suggests that genetic factors play an important role in the pathogenesis of IBD. Foreign studies have suggested that the NOD2 gene may influence the host immune response to intestinal microbes by regulating T cell function and intestinal epithelial permeability. It is now believed that most of the susceptibility genes that may be associated with IBD are involved in the regulation of the host gut immune response to microbes and the maintenance of host gut mucosal epithelial cells, microbes and immune system homeostasis. A combination of intestinal microbial communities and metabolites, host gene susceptibility, and imbalance in the natural or acquired immune response of the host intestinal mucosa are involved in the pathogenesis of IBD. Microecological agents have the function of directly supplementing or promoting the growth of host beneficial microorganisms, maintaining or adjusting the microecological balance to prevent and control diseases and enhance the health of the host. Microecological agents are safer and adverse effects are rare, mainly including probiotics, prebiotics and synbiotics. Among them, probiotic preparations are the most widely used clinically, and in recent years, research and development, the variety is increasing, and more than twenty kinds of probiotic preparations have been used clinically in China. At present, there are more studies on microecological agents for the treatment and (or) prevention of IBD. For example, the adjuvant application of microecological agents given to patients during UC remission can improve the symptoms associated with colitis and prevent postoperative recurrence, but the role of microecological agents in CD-induced remission and maintenance therapy remains unclear. The role of microecological agents in the treatment and/or prevention of IBD needs to be further validated in high-quality, multicenter randomized controlled studies.