Dysbiosis and colonic adenoma: The lethal link?

Abstract

Gut dysbiosis, a phenomenon in which the existing commensal microbiome changes to an adverse microenvironment in the colon, is thought to lead to altered cellular signals. How this is involved in producing mucosal outgrowths such as polyps in the colon is intriguing. Deciphering the various mechanisms involved provides an in-depth understanding of the link between gut dysbiosis and colonic polyps.

Key Words: Dysbiosis; Adenoma; Polyp; Gut; Microbiota

Core Tip: It is fascinating to note that the gut microbiota can be the basis for the repeated occurrence of gut pathologies such as colonic polyps. Elucidating the various mechanisms involved would provide greater insights into the problem of colonic polyps.

TO THE EDITOR

Research has taken a big leap in understanding the role of microbes in the health and wellness of individuals. Estimation of volatile organic compounds in the exhaled breath produced by the gut microbiota and excreted through the lungs can help in linking the microbiota to the underlying disease condition. This has paved the way for designing novel and innovative non-invasive screening techniques. In line with this rationale the faecal microbial marker testing is a newer addition to the existing diagnostic armamentarium of colorectal cancer screening[1,2].

Gut dysbiosis is a phenomenon of bacterial disproportion in the intestine, reflecting the alteration of the bacterial milieu in the intestine with an increase in potentially harmful facultative anaerobic bacteria replacing beneficial obligate anaerobic bacteria. It is well known that the dysbiosis is connected with local and or systemic inflammation. Whether dysbiosis triggered the event or the culmination of sequelae is subject to debate and is not clearly understood. Several consequences such as altered host immune response, increased bacterial virulence and altered post-surgical survival have been noted to result from dysbiosis[3].

The altered gut flora in dysbiosis leading to a changed host immune response can set the stage for systemic sepsis. This can also be the basis for frequent relapses in patients with Inflammatory Bowel disease. Over a period of time, the dysbiosis causing local alterations can be a forerunner in the altered cellular and molecular level signals that initiate and propagate gene mutations ultimately ending in polyps[4,5]. Studies have shown the increased presence of certain microbiota (Streptococcaceae, Lachnoclostridium, and Ralstonia) in association with polyps. When the normal gut microbiota are changed or lost, the equilibrium in the colonic microenvironment is de-stabilised to a significant extent, resulting in the increased propensity of the mucosa to develop abnormal outgrowths such as polyps which may subsequently progress to cancerous growth. Thus the influence of altered microbial metabolism, amended interaction of microbiome to host immune mechanism and varied interaction of host cells have a role to play in the mechanism of the initiation and recurrence of polyps. The challenge is in understanding the complex interaction of the modified microbiome and the colonic homeostasis[6]. Animal models have shown a prominent increase in certain bacterial species preceding the occurrence of colonic neoplasm, confirming the role of the abnormal microbiota or dysbiosis in the initiation of the trigger mechanism orchestrating the development of tumorous growth[7].

It is interesting to see how the evidence would unfold incriminating the dysbiosis and genetic mechanisms that cause recurrent colonic adenoma.