Search for dissertations about: "Yersinia thesis"
Showing result 1 - 5 of 61 swedish dissertations containing the words Yersinia thesis.
-
1. Virulence mechanisms of pathogenic Yersinia : aspects of type III secretion and twin arginine translocation
Abstract : The pathogenic bacteria Yersinia pestis and Y. pseudotuberculosis are related to the degree where the former is considered a subspecies of the latter, and still they cause disease of little resemblance in humans. Y. pestis is the causative agent of lethal bubonic and pneumonic plague, while Y. READ MORE
-
2. Antiphagocytosis by Yersinia pseudotuberculosis : role of the YopH target proteins
Abstract : The enteropathogenic bacterium Yersinia pseudotuberculosis binds to β1 integrins on a host cell via its surface protein invasin. This event stimulates signal transduction to the actin cytoskeleton of the eukaryotic cell, which allows the cell to engulf the bacterium that is attached to its surface. However, the pathogen Y. READ MORE
-
3. Persistent infection by Yersinia pseudotuberculosis
Abstract : Enteropathogenic Yersinia species can infect many mammalian organs such as the small intestine, cecum, Peyer’s patches, liver, spleen, and lung and cause diseases that resemble a typhoid-like syndrome, as seen for other enteropathogens. We found that sublethal infection doses of Y. READ MORE
-
4. Yersinia-phagocyte interactions during early infection
Abstract : Pathogenic Gram-negative Yersinia species preferentially target and inactivate phagocytic cells of the innate immune defense by translocation of effector Yersinia outer proteins (Yops) into the cells via a type III secretion system. This indicates that inactivation and avoidance of the early innate immune response is an efficient way for Yersinia species to avoid elimination and to cause diseases ranging from mild gastroenteritis (Y. READ MORE
-
5. The multifunctional GAP protein YopE of Yersinia is involved in effector translocation control and virulence
Abstract : The Gram-negative bacterium Yersinia pseudotuberculosis employs a type 3 secretion system (T3SS) to establish infections. The T3SS translocates a diverse set of effector proteins directly into the host cells. READ MORE