Fig. 3: The effects of the L-Lectin module deletion (ΔL-lectin) of the virulence factor SraP on MRSA morphology, growth, and biofilm inhibition in vitro. | npj Biofilms and Microbiomes

Fig. 3: The effects of the L-Lectin module deletion (ΔL-lectin) of the virulence factor SraP on MRSA morphology, growth, and biofilm inhibition in vitro.

From: Exploiting strong synergies between punicalagin and cefoperazone to combat methicillin-resistant Staphylococcus aureus infections

Fig. 3

Time (A) and dose (B) dependent binding kinetics and affinity of punicalagin (PA) to the purified L-lectin module from wild-type (WT) MRSA strain MW2 in vitro, as detected using surface plasmon resonance (SPR). The color of dots in B represents the PA concentrations as described in (A). RU: response or resonance unit. C Differences in cell morphology and cell wall structure of WT and ΔL-lectin MW2 strains in response to PA at 10 µg/mL as observed by transmission electron microscopy (TEM). The morphology and cell wall structure between WT and ΔL-lectin mutant were indistinguishable without PA treatment (WT vs. ΔL-lectin mutant). The L-Lectin module deletion (ΔL-lectin) did not appear to affect growth characteristics of the mutant, compared to its WT counterpart (D). However, the mutant compromised MRSA sensitivity to PA as judged by its effect on overall growth inhibition (E), adhesion (F) to host cells, and biofilm formation (G) in vitro. **P < 0.01; *P < 0.05. The number represents the mean ± SD of four replicates.

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