Abstract
Enteropathogenic bacteria have been the cause of the majority of foodborne illnesses. Much of the research has been focused on elucidating the mechanisms by which these pathogens evade the host immune system. One of the ways in which they achieve the successful establishment of a niche in the gut microenvironment and survive is by a chain of elegantly regulated gene expression patterns. Studies have shown that this process is very elaborate and is also regulated by several factors. Pathogens like, enteropathogenic Escherichia coli (EPEC), Salmonella Typhimurium, Shigella flexneri, Yersinia sp. have been seen to employ various regulated gene expression strategies. These include toxin-antitoxin systems, quorum sensing systems, expression controlled by nucleoid-associated proteins (NAPs), several regulons and operons specific to these pathogens. In the following review, we have tried to discuss the common gene regulatory systems of enteropathogenic bacteria as well as pathogen-specific regulatory mechanisms.
Highlights
Bacteria with their supposedly primitive genomic architecture, have proven to be one of the smartest living things to have existed
QseEF regulates the gene which is involved in Shiga toxins synthesis, SOS responses, and other two-component system (TCS), which includes RcsBC, PhoPQ (Reading et al, 2009, 2010; FIGURE 1 | Quorum sensing in an overview, (A) describes the AI-1 mediated Quorum sensing and its downstream target gene regulation, (B) describes the AI-2 mediated gene regulation through lsr operon, (C) Cross-kingdom communication to facilitate the bacteria to sense the cues from the host and thereby establish successful infection
That we have summarized some of the broad gene regulatory mechanisms that the enteropathogenic bacteria employ, we will discuss some of the pathogen specific mechanisms
Summary
Bacteria with their supposedly primitive genomic architecture, have proven to be one of the smartest living things to have existed. Their success of survival depends on a chain of elegantly regulated gene expression patterns. This regulation becomes all the more important in the case of pathogens, which have to cleverly sabotage the host immune responses. For successful entry and survival in the host of an enteric pathogen, these bacteria have to cross the acidic pH of the stomach, find a way to cross the barrier of the existing intestinal microbiota, escape from the cationic anti-microbial peptides and immunoglobulins in the intestine. Forty percent of the disease is reported in children under 5 years of age
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