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Articles 1 - 6 of 6
Full-Text Articles in Pathogenic Microbiology
Modulation Of Host Innate Immune Cells By Yersinia Pestis To Create A Permissive Environment For Replication., Amanda Rose Pulsifer
Modulation Of Host Innate Immune Cells By Yersinia Pestis To Create A Permissive Environment For Replication., Amanda Rose Pulsifer
Electronic Theses and Dissertations
Yersinia pestis has gained widespread infamy due to the historic outbreak during the middle ages, referred to as The Black Death. Infection with Y. pestis typically begins with deposition of Y. pestis into the dermis (bubonic plague) or respiratory tract (pneumonic plague). Tissue resident macrophages are the first innate immune cell encountered by Y. pestis. Macrophages are likely a way for Y. pestis to avoid neutrophils early in infection when the neutrophil neutralizing Type Three Secretion System is not expressed. This work focuses on which Rab host proteins are manipulated by Y. pestis, and how neutrophils are forced to …
The Surreptitious Survival Of The Emerging Pathogen Staphylococcus Lugdunensis In Macrophages Enhances S. Aureus Infection, David Watson
The Surreptitious Survival Of The Emerging Pathogen Staphylococcus Lugdunensis In Macrophages Enhances S. Aureus Infection, David Watson
Electronic Thesis and Dissertation Repository
Staphylococcus lugdunensis is an opportunistic pathogen that can cause invasive infections suggesting an ability to circumvent host immunity. S. lugdunensis was shown to resist killing and persist within macrophages and acetylation of its peptidoglycan is important for this survival. This was consistent in vivo, as S. lugdunensis resides inside Kupffer cells for at least 16 hours post-infection in mice. Despite its capability for survival, S. lugdunensis is unable to replicate within phagolysosomes. Inhibiting phagolysosomal effectors allows S. lugdunensis to initiate replication, after which the bacteria escape phagosomal containment. Moreover, intracellular S. lugdunensis augments the growth S. aureus during co-infection. Eight …
Iron And Copper Homeostasis In Staphylococcus Aureus, Holly A. Laakso
Iron And Copper Homeostasis In Staphylococcus Aureus, Holly A. Laakso
Electronic Thesis and Dissertation Repository
All microorganisms require transition metals for key metabolic processes, thus during infection microbial access to essential metals is tightly regulated by the host in a process termed nutritional immunity. Iron acquisition is critical to the pathogenesis of the formidable human pathogen, Staphylococcus aureus, which utilizes heme-uptake systems and two high-affinity iron-scavenging siderophores, staphyloferrin A (SA) and staphyloferrin B (SB) for iron acquisition. In this study, I identify sbnI as encoding a transcription factor required for expression of genes in the sbn operon, the biosynthetic operon for SB synthesis. I also show that SbnI is a novel hemoprotein, where binding …
Antibody Dependent Enhancement Of Visceral Leishmaniasis, Alan K. Mcnolty
Antibody Dependent Enhancement Of Visceral Leishmaniasis, Alan K. Mcnolty
All Master's Theses
Leishmaniasis is a parasitic disease caused by protozoans of the genus Leishmania. This vector-born disease, transmitted by biting phlebotomine sandflies, typically manifests in one of three ways. The cutaneous form of the disease is characterized by localized lesions of the skin and is by far the most common manifestation. The visceral form of the disease is caused by parasitic infiltration of internal organs, particularly the spleen, liver, and bone marrow. The mucocutaneous form is caused by parasitic infection of the mucosa in the nose or mouth. While cutaneous leishmaniasis (CL) is often self-healing, visceral leishmaniasis (VL) is fatal if …
Identification Of Host Factors Required For Yersinia Pestis Macrophage Intracellular Survival And Their Impact On Vacuole Maturation, Acidification And Trafficking., Michael Graylin Connor
Identification Of Host Factors Required For Yersinia Pestis Macrophage Intracellular Survival And Their Impact On Vacuole Maturation, Acidification And Trafficking., Michael Graylin Connor
Electronic Theses and Dissertations
Y. pestis is a facultative intracellular pathogen and the causative agent of plague. This bacterium, while most noted or the Black Death during the European 14th century, is not a historic pathogen but a re-emerging pandemic with both domestic and global impact. Y. pestis is capable of colonizing the macrophage, and actively subverts phagolysosome maturation to establish a replicative niche known as the Yersinia containing vacuole (YCV). The exploited host factors required to support the YCV are unknown. Here we identified a comprehensive list of host factors required for Y. pestis survival through a genome-wide RNAi high-throughput screen. We …
Regulation Of Rab5 Gtpase Activity During Pseudomonas Aeruginosa-Macrophage Interaction, Sushmita Mustafi
Regulation Of Rab5 Gtpase Activity During Pseudomonas Aeruginosa-Macrophage Interaction, Sushmita Mustafi
FIU Electronic Theses and Dissertations
Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen. Several antibiotic resistant strains of P. aeruginosa are commonly found as secondary infection in immune-compromised patients leaving significant mortality and healthcare cost. Pseudomonas aeruginosa successfully avoids the process of phagocytosis, the first line of host defense, by secreting several toxic effectors. Effectors produced from P. aeruginosa Type III secretion system are critical molecules required to disrupt mammalian cell signaling and holds particular interest to the scientists studying host-pathogen interaction. Exoenzyme S (ExoS) is a bi-functional Type III effector that ADP-ribosylates several intracellular Ras (Rat sarcoma) and Rab (Response to abscisic acid) small GTPases …