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Journal of Infectious Diseases & Therapy |ISSN: 2332-0877 | Volume 6
June 25-26, 2018 | Vancouver, Canada
&
3rd International Conference on
Infection, Disease Control and Prevention
2nd International Conference on
Microbial Pathogenesis & Infectious Diseases
Molecular mechanisms of hypervirulent Group A Streptococcus to evade innate immune responses and to
invade the vascular system in mouse model of pulmonary infection
Group A Streptococcus (GAS) causes common pharyngitis and occasional severe invasive infections. There is a significant
knowledge gap on why noninvasive upper respiratory GAS infections usually do not result in lower respiratory infections
while certainGAS strains can cause pneumonia and how invasive GAS disseminates systemically. A pulmonarymurine infection
model is used to address these questions. Paryngeal GAS isolates induced robust neutrophil recruitment and was effectively
cleared in a NADPH Oxidase-dependent mechansim by neutrophils. In contrast, invasive isolates with mutations in virulence
regulators CovRS and/or RopB inhibited neutrophil recruitment and caused pulmonary infections. Natural GAS RopB mutants
caused infection only in the alveolar region whereas natural CovS and RopB double GAS mutants invade the perivascular
interstitium, disrupts smooth muscle and endothelial layers of the blood vessels, and penetrates into the lumen of endothelial
layer and the systemic circulation. Correction of the CovS mutation abolished the capacity of GAS to invade the vascular
system. To identify virulecence factors that are critical for GAS innate immune evasion and vascular invasion, we tested single
and double deletion mutants of CovRS-controlled virulence genes of hypervirulent GAS. Only a surface protein was found to
be critical for the vascular invasion, and the inhibition of neutrophil recruitment requires both streptolysin S and the platelet-
activating factor acetyl hydroslase Sse. Thus, Streptolysin S- and Sse-dependent evasion of neutrophil response is critical for the
capacity of GAS to cause pulmonary infection, and GAS invasion of the vascular system requires the surface protein
Biography
Benfang Lei has completed his PhD from University of Houston, Texas and postdoctoral study at the Rocky Mountain Laboratories, NIAID, NIH at Hamilton,
Montana. He is an Associate Professor at Department of Microbiology and Immunology, Montana State University. He has published 70 primary research papers
and has been serving as an academic editor of PloS One and an editorial board member of Infection and Immunity.
Benfang Lei
Montana State University, USA
Benfang Lei, J Infect Dis Ther 2018, Volume 6
DOI: 10.4172/2332-0877-C2-040