Abstract
The mammalian gut microbial community, known as the gut microbiota, comprises trillions of bacteria, which co-evolved with the host and has an important role in a variety of host functions that include nutrient acquisition, metabolism, and immunity development, and more importantly, it plays a critical role in the protection of the host from enteric infections associated with exogenous pathogens or indigenous pathobiont outgrowth that may result from healthy gut microbial community disruption. Microbiota evolves complex mechanisms to restrain pathogen growth, which included nutrient competition, competitive metabolic interactions, niche exclusion, and induction of host immune response, which are collectively termed colonization resistance. On the other hand, pathogens have also developed counterstrategies to expand their population and enhance their virulence to cope with the gut microbiota colonization resistance and cause infection. This review summarizes the available literature on the complex relationship occurring between the intestinal microbiota and enteric pathogens, describing how the gut microbiota can mediate colonization resistance against bacterial enteric infections and how bacterial enteropathogens can overcome this resistance as well as how the understanding of this complex interaction can inform future therapies against infectious diseases.
Highlights
The resident microbes of the human gut, collectively termed as gut microbiota (Sender et al, 2016), are a highly dynamic and diverse ecosystem, estimated to be composed of trillions of microbial cells, which approximately outnumber by a ratio of 10.1 or roughly equivalent to the number of cells in the human body and encode 500 times more genes than the human genome (Li et al, 2014; Sender et al, 2016; Tierney et al, 2019; Koh and Bäckhed, 2020)
The second part is about the mechanisms of pathogenic bacteria and how pathogenic bacteria break up this resistance and colonize the gut and cause infections
There is a delicate balance in the gut microbiota population where the commensals dominate over the pathobionts/pathogens and occupy all niches and nutrients along the intestine and restrain the pathobiont overgrowth and invaded or invading pathogen colonization by having efficient metabolic pathways that outcompete the access of pathogens for the limited nutrient resource in the intestine
Summary
The resident microbes of the human gut, collectively termed as gut microbiota (Sender et al, 2016), are a highly dynamic and diverse ecosystem, estimated to be composed of trillions of microbial cells, which approximately outnumber by a ratio of 10.1 or roughly equivalent to the number of cells in the human body and encode 500 times more genes than the human genome (Li et al, 2014; Sender et al, 2016; Tierney et al, 2019; Koh and Bäckhed, 2020). The mechanisms through which the intestinal microbiota provide colonization resistance are complex and have not been fully described; many involve direct interactions (such as nutrient competition, niche exclusion, toxic substances, and metabolite production) between bacterial communities (commensals–pathogens/pathobionts), and others act by indirect mechanisms that modulate the host system physiology, the host immune response Together, these mechanisms impart to colonization resistance against exogenous pathogenic microorganisms and resident pathobionts in the gut environment (Rolhion and Chassaing, 2016; Sorbara and Pamer, 2019). The high incidence of enteric infections caused by bacterial pathogens indicates that microbiota-mediated colonization resistance can be distressed and turn ineffective Various factors such as host genetics, diet, and antibiotic usage that can alter the composition and functional capacity of the gut microbial community affect colonization resistance (Bokulich et al, 2016; Lim et al, 2017; Ducarmon et al, 2019; Pickard and Nú ñez, 2019). Typhimurium) (Theriot and Young, 2015; Rivera-Chávez and Bäumler, 2015; Abt et al, 2016), thereby rendering opportunities for pathogens to utilize disruption in colonization resistance and colonize the gut, which leads to cause infection
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