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Pathogenic Microbiology Commons

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Full-Text Articles in Pathogenic Microbiology

The Epithelial Transmembrane Protein Perp Is Required For Inflammatory Responses To S. Typhimurium Infection: A Dissertation, Kelly N. Hallstrom Oct 2015

The Epithelial Transmembrane Protein Perp Is Required For Inflammatory Responses To S. Typhimurium Infection: A Dissertation, Kelly N. Hallstrom

GSBS Dissertations and Theses

Salmonella enterica subtype Typhimurium (S. Typhimurium) is one of many non-typhoidal Salmonella enterica strains responsible for over one million cases of salmonellosis in the United States each year. These Salmonella strains are also a leading cause of diarrheal disease in developing countries. Nontyphoidal salmonellosis induces gastrointestinal distress that is characterized histopathologically by an influx of polymorphonuclear leukocytes (PMNs), the non-specific effects of which lead to tissue damage and contribute to diarrhea.

Prior studies from our lab have demonstrated that the type III secreted bacterial effector SipA is a key regulator of PMN influx during S. Typhimurium infection and that its ...


Virulence Of Group A Streptococci Is Enhanced By Human Complement Inhibitors, David Ermert, Jutamas Shaughnessy, Thorsten Joeris, Jakub Kaplan, Catherine J. Pang, Evelyn A. Kurt-Jones, Peter A. Rice, Sanjay Ram, Anna M. Blom Jul 2015

Virulence Of Group A Streptococci Is Enhanced By Human Complement Inhibitors, David Ermert, Jutamas Shaughnessy, Thorsten Joeris, Jakub Kaplan, Catherine J. Pang, Evelyn A. Kurt-Jones, Peter A. Rice, Sanjay Ram, Anna M. Blom

Open Access Articles

Streptococcus pyogenes, also known as Group A Streptococcus (GAS), is an important human bacterial pathogen that can cause invasive infections. Once it colonizes its exclusively human host, GAS needs to surmount numerous innate immune defense mechanisms, including opsonization by complement and consequent phagocytosis. Several strains of GAS bind to human-specific complement inhibitors, C4b-binding protein (C4BP) and/or Factor H (FH), to curtail complement C3 (a critical opsonin) deposition. This results in diminished activation of phagocytes and clearance of GAS that may lead to the host being unable to limit the infection. Herein we describe the course of GAS infection in ...