The opportunistic nature of gut commensal microbiota

The abundance of gut commensals has historically been associated with health-promoting effects despite the fact that the definition of good or bad microbiota remains condition-specific. The beneficial or pathogenic nature of microbiota is generally dictated by the dimensions of host-microbiota and microbe-microbe interactions. With the increasing popularity of gut microbiota in human health and disease, emerging evidence suggests opportunistic infections promoted by those gut bacteria that are generally considered beneficial. Therefore, the current review deals with the opportunistic nature of the gut commensals and aims to summarise the concepts behind the occasional commensal-to-pathogenic transformation of the gut microbes. Specifically, relevant clinical and experimental studies have been discussed on the overgrowth and bacteraemia caused by commensals. Three key processes and their underlying mechanisms have been summarised to be responsible for the opportunistic nature of commensals, viz. improved colonisation fitness that is dictated by commensal-pathogen interactions and availability of preferred nutrients; pathoadaptive mutations that can trigger the commensal-to-pathogen transformation; and evasion of host immune response as a survival and proliferation strategy of the microbes. Collectively, this review provides an updated concept summary on the underlying mechanisms of disease causative events driven by gut commensal bacteria.

Automated summary

The abundance of gut commensals has been associated with health-promoting effects, but the definition of good or bad microbiota depends on specific conditions. The interaction between host-microbiota and microbe-microbe determines the beneficial or pathogenic nature of microbiota. Emerging evidence suggests that gut bacteria, which are commonly considered beneficial, can promote opportunistic infections. This review summarizes the concepts behind the occasional transformation from commensal to pathogenic state of gut bacteria. It discusses relevant clinical and experimental studies on commensal overgrowth and bacteraemia. Three key processes and their underlying mechanisms responsible for the opportunistic nature of commensals are summarized, including improved colonisation fitness, pathoadaptive mutations, and evasion of host immune response. Overall, this review provides an updated concept summary on the underlying mechanisms of disease causative events driven by gut commensal bacteria.