Punica granatum sarcotesta lectin (PgTeL) inhibits Pseudomonas aeruginosa replication, viability, aggregation, and biofilms

Abstract

Pseudomonas aeruginosa is included in the ESKAPEE group, which includes pathogens responsible for nosocomial infections. PgTeL is a lectin from pomegranate sarcotesta active against human pathogenic microrganisms. This study evaluated the antibacterial effects of PgTeL on three strains of P. aeruginosa, one non-resistant strain (ATCC 27853) and two multidrug-resistant (MDR) strains (UFPEDA 261 and UFPEDA 262). Minimal inhibitory (MIC) and bactericidal (MBC) concentrations were determined. The anti-aggregating and antibiofilm effects of PgTeL were also evaluated as well as its synergistic effects with antibiotics. Fluorescent nanoprobes (PgTeL conjugated with quantum dots; QDs-PgTeL) were used to investigate differences in the lectin binding to the cell surface of the strains as well as possible involvement of the carbohydrate-recognizing domain (CRD) in the binding to planktonic and biofilm cells. PgTeL showed an MIC of 12.5–25.0 μg/mL, an MBC of 50.0–100.0 μg/mL and an anti-aggregating effect. Biofilm formation was inhibited by more than 50 % at PgTeL concentrations of 25.0, 3.12 and 0.78 μg/mL for ATCC 27853, UFPEDA 261, and UFPEDA 262, respectively. The lectin (0.78–3.12 μg/mL) also promoted eradication of preformed biofilms. The QDs-PgTeL conjugates revealed a higher binding efficiency of PgTeL to UFPEDA 261 (74.2 %), followed by UFPEDA262 (54.5 %) and ATCC 27853 (44.8 %). The PgTeL CRD is involved in the interaction of this lectin with planktonic or biofilm cells, as the nanoprobes had their effectiveness decreased to 8.2–21.6 % when previously incubated with fetuin. Finally, the combination of PgTeL and ceftazidime showed synergistic effects against the MDR strains (ΣFIC of 0.5 and 0.25, respectively). In conclusion, PgTeL impaired replication, viability, aggregation, and biofilm formation of P. aeruginosa and differences in the effects for the three strains may be due to distinct glycidic composition on their cell surfaces and, consequently, differential binding efficiency of PgTeL.