The role of intestinal microecology in inflammatory bowel disease and colorectal cancer: A review

Abstract

Intestinal microecology is a dominant and complex microecological system in human body. Generally, intestinal microecosystem consists of normal symbiotic flora and its living environment (including intestinal epithelial tissue and intestinal mucosal immune system). Commensal flora is the core component of microecology. Both structures of intestinal mucosa and functions of immune system are essential to maintain homeostasis of intestinal microecosystem. Under normal conditions, intestinal microorganisms and intestinal mucosa coordinate with each other to promote host immunity. When certain factors in the intestine are altered, such as disruption of the intestinal barrier causing dysbiosis of the intestinal flora, the immune system of the host intestinal mucosa makes a series of responses, which leads to the development of intestinal inflammation and promotes colorectal cancer. In this review, to further understand the relationship between intestinal microecology and intestinal diseases, we systematically elaborate the composition of the intestinal mucosal immune system, analyze the relationship between intestinal flora and mucosal immune system, and the role of intestinal flora on intestinal inflammatory diseases and colorectal cancer.

Current progresses and challenges for microbiome research in human health: a perspective

“…The balance between obligate and facultative anaerobes is essential for the integrity and function of the intestinal epithelial barrier; certain conditions, like antibiotic treatment or unhealthy lifestyles, may alter the gut microbiota composition, named dysbiosis, leading to the onset and development of different pathologies ( Naito, 2024 ). For example, the overgrowth of potentially harmful Proteobacteria , including Enterobacteriaceae , has been linked to the emergence of a pro-inflammatory microenvironment contributing to the pathogenesis of Inflammatory Bowel Diseases, as well as cancer and metabolic disorders like obesity, dyslipidaemia, type-2 diabetes, and non-alcoholic fatty liver disease ( Jia et al., 2023 ; Li et al., 2023a ). Specifically, it has been suggested that the relationship between the two dominant phyla, expressed as Firmicutes/Bacteroidetes ratio, may be associate to the development of metabolic diseases induced by high-fat diet ( Jia et al., 2023 ); also, certain bacteria in the intestine, such as Escherichia coli , Campylobacter jejuni , Fusobacterium nucleatum , and Bacteroides fragilis , have been described to express toxin proteins causing intracellular reactive oxygen species accumulation and DNA damage, and contributing to colorectal carcinogenesis ( Li et al., 2023a ).…”

“…For example, the overgrowth of potentially harmful Proteobacteria , including Enterobacteriaceae , has been linked to the emergence of a pro-inflammatory microenvironment contributing to the pathogenesis of Inflammatory Bowel Diseases, as well as cancer and metabolic disorders like obesity, dyslipidaemia, type-2 diabetes, and non-alcoholic fatty liver disease ( Jia et al., 2023 ; Li et al., 2023a ). Specifically, it has been suggested that the relationship between the two dominant phyla, expressed as Firmicutes/Bacteroidetes ratio, may be associate to the development of metabolic diseases induced by high-fat diet ( Jia et al., 2023 ); also, certain bacteria in the intestine, such as Escherichia coli , Campylobacter jejuni , Fusobacterium nucleatum , and Bacteroides fragilis , have been described to express toxin proteins causing intracellular reactive oxygen species accumulation and DNA damage, and contributing to colorectal carcinogenesis ( Li et al., 2023a ). Furthermore, changes in pH values as well as the presence of histologic alterations of the gastric mucosa, as in chronic atrophic gastritis, were also associated to increased gut dysbiosis characterized by the prevalence of oral bacteria, like Rothia mucilaginosa , Streptococcus salivarius and Granulicatella adiacens ( Filardo et al., 2022b ).…”