Journal of Infectious Diseases & Therapy
黑料网
Our Group organises 3000+ Global Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ 黑料网 Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.
黑料网 Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers
Citations : 1529
Indexed In
- Index Copernicus
- Google Scholar
- Open J Gate
- RefSeek
- Hamdard University
- EBSCO A-Z
- OCLC- WorldCat
- Publons
- Euro Pub
- ICMJE
Useful Links
Recommended Journals
Related Subjects
Share This Page
Molecular mechanisms of hypervirulent Group A Streptococcus to evade innate immune responses and to invade the vascular system in mouse model of pulmonary infection
Joint Event on 3rd International Conference on Infection, Disease Control and Prevention & 2nd International Conference on Microbial Pathogenesis & Infectious Diseases
Benfang Lei
Montana State University, USA
Keynote: J Infect Dis Ther
DOI:
Abstract
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 certain GAS strains can cause pneumonia and how invasive GAS disseminates systemically. A pulmonary murine 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 plateletactivating 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 proteinBiography
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.
E-mail: blei@montana.edu
