## 3 Results and Discussion
### Virulence of P. aeruginosa Isolated from Pre-Columbian Textiles
aeruginosa_ is pyocyanin, a blue-green pigment that alters the physiology and homeostasis of host cells by exposing it to oxidative stress. Pyocyanin modifies host cell responses by inhibiting generation of neutrophil superoxide and lymphocyte proliferation as well as by increasing interleukin-8 production by human airway epithelial cells [5]. Moreover, several host genes are induced in response to pyocyanin, including mucins, inflammatory cytokines, chemokines, and oxidative stress-responsive genes [5]. Clinical _P. aeruginosa_ strains are able to secrete pyocyanin at various levels, ranging from 1.29 to 25.94 \(\upmu\)g/mL [20]. [PERSON] et al. [21] reported less diversity in pyocyanin production in a group of clinical strains (1.62-9.83 \(\upmu\)g/mL), but the concentrations were correlated with stages of disease severity. Pyocyanin secretion also depends on strain origin, with the highest amounts in _P. aeruginosa_ isolated from the sputum and urine of patients with cystic fibrosis [20,21]. In our study, all the tested strains were able to secrete pyocyanin, but at different levels. _P. aeruginosa_ KP842564 produced 1.09 \(\upmu\)g/mL while _P. aeruginosa_ KP842565 produced 0.39 \(\upmu\)g/mL of pyocyanin (Table 2). These amounts were statistically lower than for the clinical _P. aeruginosa_ strain (8.48 \(\upmu\)g/mL). These findings are in agreement with [PERSON] et al. [9], who demonstrated the ability of all _P. aeruginosa_ isolated in their study from mineral water to produce pyocyanin, whereas 13% of clinical strains were non-pyocinotypable. Moreover, environmental _P. aeruginosa_ has been shown to secrete from 0.36 to 24.5 \(\upmu\)g/mL pyocyanin at 37 \({}^{\circ}\)C, but much higher concentrations at 30 \({}^{\circ}\)C, ranging from 1.6 to even 197.2 \(\upmu\)g/mL [6]. The virulence of _P. aeruginosa_ is also determined by exoproducts, such as proteases which help establish and maintain infections by damaging host tissues and degrading proteins that function as part of the host defenses [5]. Protease-deficient strains are generally less virulent than protease producers in burned mouse models [22]. Since proteases play an important role in _P. aeruginosa_ infections, they are typical features of clinical strains [15,23]. Among the strains tested in our study, environmental _P. aeruginosa_ KP842564 and the clinical isolate were characterized by protease production. Both strains degraded bovine serum albumin, mucin, fibrinogen, and casein, whereas the environmental strain KP842565 revealed no proteolytic activity (Table 2). Proteolysis of proteins naturally occurring in the human body should be considered as virulence attributes, but degradation of casein is also associated with _P. aeruginosa_ pathogenicity, since proteases typical for clinical isolates are capable of degrading casein [23]. The tested strains originating from textiles further exhibited hemolytic activity, forming beta hemolysins at a level statistically comparable to the clinical isolate (Table 2). Production of hemolysins indicates the ability of these strains to induce tissue damages and may play a role in spreading the infection. Clinical _P. aeruginosa_ strains are characterized by innate or acquired resistance to many antibiotic classes, including antipseudomonal penicillins, carbapenem, aminoglycos, and ciprofloxacin [24]. The resistance of this bacterium to antibiotics is the result of a number of independent co-occurring mechanisms, including restricted uptake, efflux system, drug inactivation, and changes in targets [25]. Furthermore, due to the overuse of antibiotics, the resistance of _P. aeruginosa_ is increasing globally [24]. In our study, we examined the susceptibility of the tested environmental and clinical _P. aeruginosa_ strains to antimicrobial agents from seven classes, i.e., aminoglycos, carbapenem, cephalospor, fluoroquinolones, penicillins and \(\upbeta\)-lactamase inhibitors, monobactams, and polymyxins.