Biofilm Formation in Escherichia coli

Escherichia coli (E. coli) is a versatile bacterium that can form biofilms, which are structured communities of bacterial cells enclosed in a self-produced extracellular matrix. Biofilm formation is a sequential process consisting of four main stages.

In the initial attachment phase, bacterial cells adhere to surfaces using fimbriae (pili), flagella, and adhesins such as curli fibers and type 1 fimbriae (Beloin et al., 2008). This attachment is influenced by hydrophobic interactions and electrostatic forces. In the microcolony formation stage, bacteria multiply and secrete an extracellular polymeric substance (EPS) composed of polysaccharides, proteins, DNA, and lipids, which facilitates bacterial aggregation (Guilhen et al., 2017). The biofilm maturation phase is characterized by the development of multilayered bacterial structures within the EPS matrix, with the formation of channels that allow for nutrient and oxygen distribution. Quorum sensing (QS) plays a critical role in biofilm regulation by controlling gene expression and enhancing biofilm stability (Li et al., 2014). Finally, in the dispersion phase, bacterial cells detach due to environmental changes, allowing colonization of new surfaces (Monds & O’Toole, 2009).

Several factors regulate biofilm formation in E. coli. One of the key regulators is quorum sensing (QS), which utilizes autoinducer-2 (AI-2) signaling. This process allows for communication between different species and controls the production of extracellular polymeric substances (EPS) as well as motility (Miller & Bassler, 2001). Another critical pathway is the cyclic di-GMP (c-di-GMP) pathway. High levels of c-di-GMP promote biofilm formation, while low levels enhance motility (Hengge, 2009). Environmental conditions also significantly influence biofilm formation. For example, a neutral to slightly acidic pH and optimal temperatures around 37°C promote biofilm growth (Pratt & Kolter, 1998). Additionally, nutrient availability is crucial, as nutrient limitation can trigger biofilm formation as a survival strategy (O'Toole et al., 2000).

Biofilm formation in E. coli has significant implications in both clinical and industrial settings. In the medical field, biofilm-forming E. coli strains are responsible for urinary tract infections (UTIs), catheter-associated infections, and gastrointestinal diseases, which are challenging to treat due to increased antibiotic resistance within biofilms (Donlan & Costerton, 2002). In industrial settings, biofilms pose contamination risks in food processing units, water pipelines, and medical devices, leading to hygiene and safety concerns (Shi & Zhu, 2009). To combat E. coli biofilms, various antibiofilm strategies have been explored. Enzymatic treatments, such as DNase and dispersing B, have been used to degrade the EPS matrix and disrupt biofilms (Kaplan, 2010). Natural compounds like quercetin and curcumin have also demonstrated biofilm inhibition properties (Kerekes et al., 2013). Additionally, quorum-sensing inhibitors targeting AI-2 signaling can prevent bacterial communication, thereby reducing biofilm formation (LaSarre & Federle, 2013). Surface modifications, including anti-adhesive coatings on medical devices, have also been developed to prevent bacterial attachment (Ribeiro et al., 2012).

References

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