Study of the IgG endoglycosidase EndoS in group A streptococcal phagocyte resistance and virulence
Author Information
Author(s): Jonathan Sjögren, Cheryl YM Okumura, Mattias Collin, Victor Nizet, Andrew Hollands
Primary Institution: Lund University
Hypothesis
EndoS contributes to GAS virulence by hydrolyzing the N-linked glycan on IgG and thereby impairing antibody mediated functions in the immune system.
Conclusion
In a highly virulent M1T1 background, EndoS has no significant impact on GAS phagocyte resistance and pathogenicity, but high levels of EndoS expression may contribute to virulence in certain GAS strains.
Supporting Evidence
- Knocking out the EndoS gene in GAS M1T1 background revealed no significant differences in bacterial survival in immune cell killing assays.
- Exogenous addition and heterologous expression of EndoS increased GAS resistance to killing by neutrophils and monocytes in vitro.
- Heterologous expression of EndoS in M49 GAS increased mouse virulence in vivo.
Takeaway
The study looked at how a specific enzyme from bacteria affects their ability to resist immune cells. It found that this enzyme doesn't help the most dangerous bacteria survive, but it might help other types of bacteria.
Methodology
The study used targeted allelic replacement mutagenesis and heterologous expression to investigate the role of EndoS in GAS phagocyte resistance and pathogenicity in vitro and in vivo.
Limitations
The study's findings may be limited by the specific mouse model used and the expression levels of EndoS during murine infection.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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