Molecular Microbiology Research, 2025, Vol.15, No.1, 18-27 http://microbescipublisher.com/index.php/mmr 19 the intestinal flora and are helpful for physical health (Jang et al., 2017). E. coli has many genetic changes and strong adaptability, so it can live in many different environments and is easy to obtain drug resistance (Ramos et al., 2020). This change mainly comes from its instability in the genome structure, which often "borrows" new genes from other bacteria, which makes it easier to adapt to the new environment. 2.2 Commensal E. coli and its role in the human microbiome Most E. coli are actually "good bacteria" and are frequent visitors in our bodies and mainly live in the intestines. They “cooperate with our bodies” and benefit each other. About 90% of E. coli strains are such symbionts that generally do not cause disease (Ramos et al., 2020). These "good bacteria" can help us digest food and synthesize some vitamins, which are very useful for maintaining intestinal health. They can also prevent bad bacteria from “setting up” in the intestines (Jang et al., 2017). However, if the intestinal inflammation or the bacterial flora is imbalanced, E. coli may grow excessively and sometimes become “bad bacteria”, causing problems (Winter et al., 2013; Kittana et al., 2018). 2.3 Mechanisms of E. coli colonization in the gut Escherichia coli can "set up" in the intestine by sticking to the mucus layer of the colon. It has many ways to adapt to the environment of the gut and maintain its "turf". One important advantage is its facultative anaerobic properties. When intestinal inflammation it can breathe with nitrates produced by the body, which can outperform other bacteria (Winter et al., 2013). In addition, it also relies on a mechanism called "group sensing" (QS) to control the expression of virulence factors, that is, to determine whether it wants to become bad. This mechanism relies on the use of signal substances between bacteria, such as SdiA protein, autoinducers AI-2, AI-3 and indole (Figure 1) (Mayer et al., 2023). It also responds to changes in the environment and interacts with the human immune system, which makes it stay more stable in the intestines and is not easily removed (Kittana et al., 2018; Denamur et al., 2020). Figure 1 Schematic representation of the LuxR-type QS system in E. coli (Adopted from Mayer et al., 2023) Image caption: Although E. coli does not present a synthase that produces AHLs (green hexagon), it can sense these QS signals produced by other bacterial species. Through the orphan SdiA regulator, E. coli can induce a signalling to regulate the expression of several genes, including the ftsQAZ operon, in a cellular density-dependent manner. Effects on E. coli virulence-associated genes and phenotypes mediated by the LuxR solo regulator SdiA are shown. Green arrows indicate positive regulation, red lines indicate gene or phenotype inhibition, and blue lines indicate a link between different phenotypes. Biofilm regulation by SdiA is a controversial point in the literature as explained below. Although SdiA plays a role in drug resistance regulation, the effect of AHLs on this phenotype (dotted line) needs to be confirmed (Adopted from Mayer et al., 2023)
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