Effects of four antibiotics on Pseudomonas aeruginosa motility, biofilm formation, and biofilm-specific antibiotic resistance genes expression

Antibiotic resistance generally refers to an increase in the minimum inhibitory concentration (MIC) of an antibiotic due to a permanent change in bacteria, such as resistance acquired through mutation or horizontal gene transfer [1]. Bacteria can become resistant to antibiotics through mutational changes, horizontal gene transfer, and the acquisition of resistance genes. Resistance by mutational changes can result in decreased antibiotic uptake, modification of antibiotic targets, overexpression of secretory pumps, and antibiotic-inactivating enzymes. Additionally, biofilm formation mechanisms are associated with antibiotic resistance [2].

Biofilms usually contain different species of microorganisms and secreted polysaccharides, extracellular DNA (e-DNA), and proteins. The number of studies on biofilms has been increasing rapidly in recent years due to the adverse effects of biofilms on human health. Unlike planktonic cells, biofilm cells are 10 to 1000 times more resistant to antibiotics [3,4]. Medically significant biofilms can form on dental plaque, ear infections, heart valves, catheters, and implant surfaces, as well as on living or nonliving surfaces in diseases such as cystic fibrosis. Currently, it is estimated that more than 60% of human infections are caused by biofilms [5]. Therefore, it is essential to discover new antibiofilm agents and understand biofilm resistance mechanisms.

P. aeruginosa is one of the common causes of bacterial infection in humans, animals, and plants worldwide, and it is an opportunistic multidrug-resistant pathogen that manifests itself, especially in hospital-acquired infections and immunocompromised patients [6,7]. P. aeruginosa cells in its biofilm growth state are significantly more resistant to antimicrobial agents than in its planktonic state [8]. Its biofilm structure includes physical or chemical diffusion barriers to antimicrobial penetration into the biofilm, the slow growth of the biofilm due to nutrient restriction, the activation of a general stress response, and the emergence of a biofilm-specific phenotype [9].

Biofilm-specific antibiotic resistance is a concept of biofilm resistance. To our knowledge, this topic, first proposed by George O'Toole and Thien-Fah Mah, seeks to elucidate the molecular mechanisms underlying the antibiotic resistance of biofilms [9]. Given the heterogeneous nature of biofilms, multiple resistance and/or tolerance mechanisms must act together to provide an overall high level of resistance [10]. Changes in the expression levels of certain genes (ndvB, tssC1, PA0756–0757, PA1875–1877, PA5033, and PA2070) in P. aeruginosa biofilm structures have been reported in the literature to cause biofilm-specific antibiotic resistance [8].

In this study, we investigated the effects of 4 clinically used antibiotics, which are tobramycin, fosfomycin, ciprofloxacin, and piperacillin/tazobactam, on the motility of PAO1, the attachment of cells, and the expression levels of selected biofilm-specific antibiotic resistance genes (ndvB, tssC1, PA5033, and PA2070). Consequently, it was aimed to understand motility, biofilm formation, and biofilm-specific antibiotic resistance gene expressions in the PAO1 P. aeruginosa strain treated with antibiotics.

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