Gut microbiome diversity major cause of IBD

Inflammatory Bowel Disease (IBD) is all about disruptions in the intestines. It arises when the immune system mistakenly attacks healthy cells in the bowel causing inflammation, sometimes chronic. IBD includes Crohn's Disease (CD) and Ulcerative Colitis (UC), both characterised by inflammation. Symptoms are abdominal pain, weight loss, and changes in bowel movement. In short, issues in the gut lead to IBD.

The first IBD, something like UC today, was recorded in the late 1700s. The term ‘ulcerative colitis’ was first coined in 1859. However, in 1932, CD was distinguished from UC owing to its transmural and often patchy pattern of inflammation in any part of the GI tract But UC is restricted to the colon, typically starting from the rectum and spreading proximally to the cecum in many patients.

Studies say that abnormal immunological responses to the gut microbiota play a crucial role in IBD susceptibility and progression. Therefore, gut microbiota acts as a metabolic organ and contributes to health through its role in various physiological functions. It has been shown that composition of the gut microbial communities is critically different between healthy individuals and IBD patients.

Gut microbiome diversity plays a key role in IBD. Changes of the gut microbiota, commonly referred to as ‘gut dysbiosis, (function that promote potential disease states) are being delved upon to develop strategies for prognosis and treatment of the disease

Though CD and UC have common symptoms, their pathobiology regarding the spatial distribution and penetrance of inflammation along the intestine and therapeutic responses are different. 

Proper understanding of such differences and associated metabolic changes may help devise novel therapeutic intervention strategies.

In the studies conducted, scientists examined faecal metagenomics sequencing data taken from CD and UC patients from five developed nations with IBD prevalence. However, this  does not represent region-specific gut microbiota. Outcomes after analysing the faecal metagenomics data and associated disease metadata to identify microbial associations with CD, UC and healthy controls were subjected to ‘in silico’ community modelling and metabolic pathway construction. Overall, despite the known diversity of the gut microbial communities, consistent differences were found in the gut microbiota of CD and UC patients. The gut microbial metabolic modelling further suggested disease specificity in the microbial metabolic fluxes/pathways for CD versus UC. The finding help understand microbial dysbiosis in CD and UC patients and develop effective diagnostic and therapeutic strategies.

Further, the alpha diversity (Shannon diversity) and beta diversity (Bray-Curtis), the primary types of diversity explored in microbial ecology, of the IBD datasets were calculated and other tests done to assess the diversity of statistically significant species between UC, and CD. In most cases UC recorded higher diversity over CD. 

Though it was mooted that transmissible bacterial could cause IB in 1900s, research proved otherwise, that no pathogens in the traditional sense have been found for causing IBD. Few studies have examined the role fungi and viruses in the gut in causing IBD.  

Thus, scientists believe that indigenous gut microbes, when given the opportunity, can transform, trigger, and contribute to the etiopathogenesis of IBD.

IBD cases have been on the rise with change in way of life, industrialisation, urbanisation of modern societies, technological influence among other causes. Besides the non-inheritable factors, such as environs, mental, move from plant-based to animal-based processed diets, smoking and antibiotic administration. As faecal matter is not region specific, scientists are taking endoscopic approaches to acquire region-specific samples. However, scientists are still digging into the aetiology of IBD with the support of advancing technology to come up with microbiome-based diagnostics and interventions.