Streptococcal collagen‐like protein (Scl‐1) promotes resistance to phagocytic killing of group A Streptococcus (836.2)

Abstract

The up‐regulation of the gene encoding Streptococcal collagen‐like protein (scl‐1) in invasive Group A Streptococcus has been hypothesized to promote bacterial resistance to host defenses. Our previous data demonstrated that when incubated with phagocytic cells, an scl‐1 mutant strain exhibits significantly decreased survival compared to wild‐type and plasmid‐complemented strains. In our current study, we have collected results that support two possible molecular mechanisms by which Scl‐1 contributes to bacterial evasion of phagocytic killing. First, the surface protein Scl‐1 may serve as a physical barrier to mediate resistance to antimicrobial molecules contained in phagocytic cell granules. Scl‐1 directly contributes to bacterial resistance to the antimicrobial peptide human cathelicidin LL‐37, granule proteases and reactive oxygen species, though Scl‐1 does not affect peroxide production by phagocytic cells per se. Secondly, Scl‐1 contributes to bacterial survival by suppression of degranulation and release of antimicrobial molecules, and consequently the formation of neutrophil extracellular traps (NETs). Thus, the results show that Scl‐1 is a multi‐faceted virulence factor that mediates bacterial evasion to phagocytic killing by both suppressing the host response and by mediating direct resistance to antimicrobial molecules.