## 1 Introduction  
_Pseudomonas aeruginosa_ (PAO1) is a Gram-negative opportunistic bacteria associated with acute and chronic infections in humans; it is not only linked to hospital-acquired infections but also to individuals with conditions such as immunodeficiency virus infection, cancer, severe burns, immunologic genetic diseases, and diabetes mellitus, as well as other underlying health concerns [1; 2]. Over the course of recent years, there has been a notable escalation in the prevalence of _P. aeruginosa_ strains that are resistant to a range of drug substances, including trimethoprim, chloramphenicol, cephalosporporins, macrolides, tetracyclines, and fluoroquinolones [2]. Inside the quinolones, the most effective antibiotic reported for _P. aeruginosa_ is ciprofloxacin (CIP). Ciprofloxacin has a bactericidal effect by inhibiting the bacterial DNA topoisomerase and gyrase. Worldwide reports have been describing a decrease in the overall susceptibility of _P. aeruginosa_ and CIP remains within the small group of antibiotics administered to treat _P. aeruginosa_ infections via oral [3]. The increase in the drug-resistant strains of _P. aeruginosa_ has garnered significant attention from the global medical community, highlighting not only the need to perceive the mechanisms behind the resistance mechanisms to conventional drugs but also to discover new strategies to deal with these pathogens [2]. One important bacterial resistance mechanism is the formation of biofilms. Biofilms are structures composed of extracellular components secreted by bacterial cells that lower the penetration of antimicrobial drugs in bacteria cells [4; 5; 6; 7; 8; 9]. Therefore, biofilms increase the bacterial survival rate in adverse environments [7]. In a study, 63 cases of carbapenem-resistant _P. aeruginosa_ were evaluated on their capacity to form biofilms as a predictive factor for mortality. In the described study, [PERSON] et al. found that an increase of just one percent in the biofilm production in these strains could increase the risk for mortality in patients suffering from bacteremia 1.10 times [10]. To overcome bacterial resistance and pathogenicity, new strategies have been studied, with three of them being the inhibition or modulation of the quorum sensing (QS), the use of QS inhibitors [11] or gene mutations [1], and the use of phage therapy [4; 11]. The opportunist pathogen PAO1 carries the capacity to coordinate the whole bacterial population by cell-to-cell communication, which is also called QS. The expression of QS is often increased proportionally to the increase in the bacterial population. Therefore, the modulation of QS benefits bacterial survival and adaption to stressful environments, due to the expression of PAO1 virulence traits and biofilm formation. These traits are regulated by two acyl-homoserine lactoses, LasI/LasR, and PQS-MvftR [6; 7; 8; 9]. The N-acyl homoserine lactones are signal molecules that control de production of proteases, hemolysis, chitinases, lipases, siderophores, extracellular r DNA, and extracellular polysaccharides [2; 4; 8]. Modifications on either _las_R (protease and elastase) or _las_l (auto inducer) in the strains of PAO1 lower the expression of the QS system genes, the virulence traits, and the biofilm formation. The virulence traits of PAO1 can be observed in Figure 1. Therefore, the modulation of the QS is known as anti-virulence therapy [8]. A study, conducted by [PERSON] et al., showed a reduction of 65% in proteases, 22% in elastases, and 32% in pyocyanins by applying QS inhibitors in PAO1 cells [12]. The virulence traits of PAO1 can be divided into functional groups based on the bacteria function in the cell, as seen in Figure 2. One of these groups is the proteases. Proteases are composed of a signal peptide, a pro-peptide, and a mature protease domain. They are firstly expressed and then processed twice to reach their mature form by cleavage processes during the translocation on the cytoplasmatic membrane and secondly in the periplasm [13].