|ANDREOZZI, ELISA - Collaborator|
|Gunther, Nereus - Jack|
|ROTUNDO, LUCA - University Of Urbino|
Submitted to: Frontiers in Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/5/2018
Publication Date: 11/23/2018
Citation: Andreozzi, E., Gunther, N.W., Reichenberger, E.R., Cottrell, B.J., Rotundo, L., Nunez, A., Uhlich, G.A. 2018. Pch genes control biofilm and cell adhesion in a clinical serotype O157:H7 isolate. Frontiers in Microbiology. 9(2829). https://doi.org/10.3389/fmicb.2018.02829.
Interpretive Summary: The foodborne pathogen known as Shiga toxin-producing Escherichia coli (STEC) produces structures on its surface called curli fimbriae. Curli are an important component of biofilm (a complex structure consisting of bacteria and other material adhering to a surface) formation that increases the resistance of the pathogen to environmental stresses. Curli fimbriae are also involved in adhesion to human cells but most clinical STEC strains produce only small amounts of curli, likely as an adaptive response to avoid recognition by the human host. In this study, we show that a gene known as pchE controls the presence of adhesion factors, including curli, and helps maintain bacterial adhesion to host cells under less stressful conditions. However, exposure to certain antibiotics decreases pchE expression, resulting in a higher level of cell adhesion and activation of other bacterial virulence (disease causing ability) factors. This study provides information to design targeted therapies that will prevent pchE activity and cell adhesion, which would be a new method for control of this pathogen.
Technical Abstract: In a previous study, induction of the Escherichia coli serotype O157:H7 SOS response decreased csgD expression in clinical isolate, PA20, at 30°C but strongly induced genes in the horizontally-transferred-DNA regions (HTR), including many virulence regulators. To determine the role of HTR regulators in csgD and curli fimbriae control, certain regulators were plasmid-expressed in wild-type and mutant strains of PA20 and its strong biofilm-forming derivative, 20R2R. The O157:H7 group 3 perC homologue, pchE, strongly repressed csgD and CsgD-dependent phenotypes such as biofilm formation and Congo red dye affinity in a ler-independent manner at 30 deg C. At 37 deg C under non-SOS inducing conditions, curli, rather than espA, contributed to host cell adhesion and pchE was capable of minimizing curli-dependent cell adhesion, providing a host-adapting regulatory control mechanism for the adhesive phenotype. During induction at 37 deg C, pchE was repressed, allowing curli expression during the group1 pch initiation of EspA-dependent intimate adhesion.