{"id":{"repo_id":"buffalo","oai_identifier":"oai:ubir.buffalo.edu:10477/80851"},"canonical_url":"https://search.dev.ndltd.org/etd/buffalo/oai:ubir.buffalo.edu:10477/80851","repository":{"repo_id":"buffalo","name":"Buffalo","base_url":"https://ubir.buffalo.edu/oai/request"},"display":{"title":"Oral Bacteria Modulate Killing of Candida albicans by Phagocytic Cells","abstract":"Ph.D.","abstract_html":"Ph.D.","abstract_has_math":false,"creators":["Salvatori, Ornella"],"institution":"State University of New York at Buffalo","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Edgerton, Mira","Oral Biology"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-10-29T16:47:33Z","date_published":"2019-10-29T16:47:33Z","updated_at":"2026-07-27T19:05:25Z","subjects":["microbiology","immunology"],"languages":["eng"],"rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10477/80851","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Edgerton, Mira","Oral Biology"]},{"key":"dc:creator","label":"Author","values":["Salvatori, Ornella"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2019-10-29T16:47:33Z","2019","2019-07-16 13:44:06"]},{"key":"dc:publisher","label":"Institution","values":["State University of New York at Buffalo"]},{"key":"dc:type","label":"Dc Type","values":["Text","Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["microbiology","immunology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/10477/80851"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Ph.D.","Candida albicans is an opportunistic fungal pathogen colonizing the mucosa of healthy hosts and is the major causative agent of oropharyngeal candidiasis. Its behavior can be modified by the innate immunity and the presence of microbial flora. As part of the host innate immune system, phagocytic cells are crucial players in initial defense against Candida albicans infection. In turn, C. albicans utilizes MAPKinases and Ras1-cAMP stress response signaling pathways to protect itself from killing. We began this study by testing the importance of MAPKinase pathways on C. albicans phagocytosis by neutrophils and subsequent phagosomal survival (Chapter 1). Phagocytosis was influenced by C. albicans morphology, so that hyphal length > 10 μm reduced the phagocytic index in human neutrophils. Primary human neutrophils were significantly more efficient in killing phagocytosed C. albicans, compared to their mouse counterpart. We found that both C. albicans Cek1 and Hog1 pathways were required for survival of phagocytosed yeast, whereas deletion of C. albicans RAS1 resulted in a significantly increase in survival within neutrophils. We hypothesized that this resistant phenotype was as result of an increase resistance to oxidative and non-oxidative killing mechanisms of neutrophils. The absence of Ras1 reduced almost completely ROS release by neutrophils. Moreover, C. albicans Δ/Δras1 cells had increased resistance to hydrogen peroxide as a result of high levels of catalase activity. This phenotype was specific to Ras1, since these effects were not observed in the absence of its partner Cyr1 or with its downstream target Efg1."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Oral Bacteria Modulate Killing of Candida albicans by Phagocytic Cells"]}]}],"canonical_facts":{"dc:contributor":["Edgerton, Mira","Oral Biology"],"dc:creator":["Salvatori, Ornella"],"dc:date":["2019-10-29T16:47:33Z","2019","2019-07-16 13:44:06"],"dc:description":["Ph.D.","Candida albicans is an opportunistic fungal pathogen colonizing the mucosa of healthy hosts and is the major causative agent of oropharyngeal candidiasis. Its behavior can be modified by the innate immunity and the presence of microbial flora. As part of the host innate immune system, phagocytic cells are crucial players in initial defense against Candida albicans infection. In turn, C. albicans utilizes MAPKinases and Ras1-cAMP stress response signaling pathways to protect itself from killing. We began this study by testing the importance of MAPKinase pathways on C. albicans phagocytosis by neutrophils and subsequent phagosomal survival (Chapter 1). Phagocytosis was influenced by C. albicans morphology, so that hyphal length > 10 μm reduced the phagocytic index in human neutrophils. Primary human neutrophils were significantly more efficient in killing phagocytosed C. albicans, compared to their mouse counterpart. We found that both C. albicans Cek1 and Hog1 pathways were required for survival of phagocytosed yeast, whereas deletion of C. albicans RAS1 resulted in a significantly increase in survival within neutrophils. We hypothesized that this resistant phenotype was as result of an increase resistance to oxidative and non-oxidative killing mechanisms of neutrophils. The absence of Ras1 reduced almost completely ROS release by neutrophils. Moreover, C. albicans Δ/Δras1 cells had increased resistance to hydrogen peroxide as a result of high levels of catalase activity. This phenotype was specific to Ras1, since these effects were not observed in the absence of its partner Cyr1 or with its downstream target Efg1."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/10477/80851"],"dc:language":["eng"],"dc:publisher":["State University of New York at Buffalo"],"dc:rights":["Users of works found in University at Buffalo Institutional Repository (UBIR) are responsible for identifying and contacting the copyright owner for permission to reuse. University at Buffalo Libraries do not manage rights for copyright-protected works and cannot assist with permissions.","Copyright retained by author."],"dc:subject":["microbiology","immunology"],"dc:title":["Oral Bacteria Modulate Killing of Candida albicans by Phagocytic Cells"],"dc:type":["Text","Dissertation"]},"updated_at":"2026-07-27T19:05:25Z"}