Contribution of the Gut Microbiome to the Perpetuation of Inflammation in Crohn's Disease: A Systematic Review

Abstract

Crohn's disease (CD) is a sub-type of inflammatory bowel disease (IBD) with a characteristic relapsing and remitting inflammation involving the gastrointestinal (GI) tract. Although there are several medications to relieve the symptoms, there is no definite cure for the condition. This paper highlights how CD affects our gut flora, which subsequently leads to the perpetuation of inflammation. This review was conducted according to Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) 2020 guidelines using PubMed, ScienceDirect, Multidisciplinary Digital Publishing Institute (MDPI), and Google Scholar as sources for relevant literature. After applying the quality appraisal tools, we finalized 11 articles for the paper. Inflammation seen in CD leads to dysbiosis, where there is a reduction in beneficial microbes such as Faecalibacterium and Roseburia species and an increase in pathogenic microbes such as Escherichia and Proteus species. This difference in gut microbes disrupts barrier function and immune processes in the intestine, contributing to the worsening of inflammation seen in CD. Several studies have been carried out to understand this complex relationship between the gut microbiome (GM) and CD, as it may serve as a potential novel therapeutic alternative, necessary as CD's burden is increasing globally.

Keywords: crohn’s disease; disease progression; dysbiosis; gut microbiome; inflammation.

Figure 1. PRISMA flowchart

PRISMA: Preferred Reporting Items for Systematic Reviews and Meta-analysis; MDPI: Multidisciplinary Digital Publishing Institute; n: total number

Figure 2. Immune cells in CD

Image credits: Sai Pavitra Paidimarri CD: Crohn's disease; IL-1β: interleukin 1 beta cell; γδ T cell: gamma delta T cell; IFN-γ: interferon-gamma cell; TNF-α: tumor necrosis factor-alpha cell; Th: T-helper; NKT: natural killer T-cells; ILC-3: type 3 innate lymphoid cells