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Streptococcal collagen‐like protein 1 shields group A Streptococcus from antimicrobial molecules (836.8)
Author(s) -
Shimamoto Jacqueline,
Doehrmann Simon,
Etesami Neelou,
Martin Gary,
Nizet Victor,
Okumura Cheryl
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.836.8
Subject(s) - virulence , microbiology and biotechnology , antimicrobial , streptococcus pyogenes , bacteria , virulence factor , streptococcus , biology , immune system , bacterial outer membrane , mutant , phagocytosis , staphylococcus aureus , immunology , escherichia coli , biochemistry , gene , genetics
Group A Streptococcus causes a spectrum of diseases ranging from pharyngitis to life‐threatening diseases such as streptococcal toxic shock‐like syndrome. Invasive strains of GAS increase the expression of virulence factors that promote bacterial survival in the face of the human immune system. One such virulence factor is Scl‐1, a surface collagen‐like protein that has been shown in other less virulent strains to mediate attachment and resistance to serum factors. Previous work in our lab demonstrated that Scl‐1 plays a role in bacterial survival against phagocytes, but the molecular mechanism for this enhanced survival has not been determined. In the current work, we determined that the presence of Scl‐1 promotes resistance to phagocytic antimicrobial factors such as peroxide. We then used transmission electron microscopy (TEM) to examine whether Scl‐1 can act as a physical barrier to antimicrobial molecules. Preliminary analysis of wild‐type, scl‐1 mutant, and plasmid‐complemented strains suggests differences in the cell wall density of the scl‐1 mutant strain. TEM analysis of peroxide‐treated strains also suggests that Scl‐1 provides a physical barrier to protect the bacterial membrane from oxidative damage. Thus, Scl‐1 contributes to the virulence of the bacteria by acting as a molecular “shield” to protect the bacteria from antimicrobial molecules produced by phagocytic cells.