Table 2 Cell surface hydrophobicity of Lactococcus strains Lactoc

Table 2 Cell surface hydrophobicity of Lactococcus strains Lactococcus Strain Actual Value† Hydrophobicity Index‡ L. lactis 1363 WT 59.7 ± 7.2 100 L. lactis 1363::pJRS525 56.6 ± 5.5 98 L. lactis 1363::pSl230 82.0 ± 2.6 **137 † Actual hydrophobicity values were calculated based on hexadecane binding as described in Methods. Values are representative of three separate experiments with ten replicates ± SD ‡ Hydrophobicity Index represents the ration of actual hydrophobicity value for each strain to that of the isogenic wild-type (WT) strain multiplied by 100 ** Asterisks denote a statistically significant difference of Δscl1 mutants versus

WTs at P ≤ CBL0137 datasheet 0.001 Discussion Group A Streptococcus strains vary because of the vast number of M-protein types, and this variation is associated with varying frequency of isolation and exacerbation of disease [40, 41]. The M41-, M28-, M3-, and M1-type strains selected for the current study represent a significant intraspecies diversity among clinical Selleck XAV-939 isolates of GAS. M41 GAS was a major causative agent of superficial skin infections [42–44], and strain MGAS6183, harboring the Scl1.41 protein, has been studied extensively [19, 21, 22]. M28-type GAS (strain MGAS6143) has historically been associated with puerperal fever and currently is responsible for extensive human infections world-wide [45]. M1T1 GAS, represented

by strain MGAS5005, is a globally disseminated clone responsible for both pharyngitis and invasive infections [46–48]. The M3-type strains of GAS cause a disproportionally large number of invasive GAS infections PLEKHM2 that are responsible for traumatic morbidity and death [49, 50]. Initial studies by Lembke et al. that characterized biofilm formation among various M types of GAS typically included several strains of the same M type [1, 28]. These studies reported a significant strain-to-strain variation in ability to form biofilms within each M type. Studies that followed compared biofilm formation by defined isogenic WT and mutant strains to assess the

contribution of specific GAS surface components responsible for a biofilm phenotype, including M and M-like proteins, hyaluronic acid capsule, lipoteichoic acid, and pili [12, 13]. In the current study, we have assessed the role and contribution of the surface protein Scl1 in the ability to support biofilm formation by GAS strains of four distinct M types. Recent Z-IETD-FMK mouse advances in molecular mega- and pathogenomics has enabled the characterization of numerous M3-type strains with a single nucleotide resolution [51, 52]. Interestingly, all five M3-type strains MGAS158, 274, 315, 335, and 1313 that were originally used for scl1-gene sequencing [14], plus an additional strain MGAS2079 (not reported) harbor the same scl1.

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