{"id":1438,"date":"2017-12-09T02:50:51","date_gmt":"2017-12-09T02:50:51","guid":{"rendered":"http:\/\/depts.washington.edu\/cfrtc\/?p=1438"},"modified":"2017-12-14T23:10:16","modified_gmt":"2017-12-14T23:10:16","slug":"past-fellow-reichhardt","status":"publish","type":"post","link":"https:\/\/depts.washington.edu\/cfrtc\/past-fellow-reichhardt\/","title":{"rendered":"Past Fellow &#8211; Reichhardt"},"content":{"rendered":"<p>[et_pb_section fullwidth=&#8221;on&#8221; specialty=&#8221;off&#8221;][et_pb_fullwidth_slider admin_label=&#8221;Fullwidth Slider&#8221; show_arrows=&#8221;on&#8221; show_pagination=&#8221;on&#8221; auto=&#8221;off&#8221; parallax=&#8221;off&#8221; parallax_method=&#8221;off&#8221; module_id=&#8221;interior&#8221;][et_pb_slide background_image=&#8221;https:\/\/depts.washington.edu\/cfrtc\/wp-content\/uploads\/2014\/12\/microscope.jpg&#8221; background_color=&#8221;#ffffff&#8221; alignment=&#8221;center&#8221; background_layout=&#8221;dark&#8221; \/][\/et_pb_fullwidth_slider][\/et_pb_section][et_pb_section][et_pb_row][et_pb_column type=&#8221;1_4&#8243;][et_pb_sidebar admin_label=&#8221;Fellowships Sidebar&#8221; orientation=&#8221;left&#8221; area=&#8221;et_pb_widget_area_11&#8243; background_layout=&#8221;light&#8221; \/][\/et_pb_column][et_pb_column type=&#8221;3_4&#8243;][et_pb_text admin_label=&#8221;Past Fellow Reichhardt text&#8221; background_layout=&#8221;light&#8221; text_orientation=&#8221;left&#8221;]<\/p>\n<h1 style=\"text-align: center;\">Regulation of <em>Pseudomonas aeruginosa<\/em> biofilm structural integrity by the matrix protein CdrA<\/h1>\n<p>Fellow: <a href=\"https:\/\/microbiology.washington.edu\/postdoc\/current-fellows\">Courtney Reichhardt, PhD<br \/>\n<\/a>Microbiology<\/p>\n<p>Mentor: \u00a0<a href=\"https:\/\/microbiology.washington.edu\/users\/matthew-r-parsek\">Matthew Parsek, PhD<br \/>\n<\/a>Professor,\u00a0Microbiology<\/p>\n<p>Most bacteria assemble and persist as biofilms, which are multicellular communities encased in a biopolymerrich matrix. In the human host, biofilms often confer resistance to antibiotics and contribute to serious and chronic infections including lung infections in patients with cystic fibrosis (CF). In particular, <em>Pseudomonas aeruginosa<\/em> is implicated in the majority of lung infections in adult patients with CF. The formidable survival traits of biofilms combined with our dwindling pipeline of effective antibiotics make it imperative that we undertake in-depth analyses to improve our understanding of biofilms. Biofilms form three-dimensional structures that are robust enough to resist clearance by the immune system and medical treatment but also can readily disassemble to allow bacteria to infect new sites. Many questions of how bacteria and matrix molecules interact to form these structures remain unanswered. This proposed research will investigate the maintenance and regulation of <em>P. aeruginosa<\/em> biofilm structural integrity with a specific focus on a key biofilm matrix protein called CdrA. CdrA was the first biofilm matrix protein discovered in <em>P. aeruginosa<\/em>, and it has been shown to contribute to biofilm stability. The hypothesis is that CdrA acts in part by serving as a tether between cells and the biofilm matrix that can be cut to initiate biofilm dispersal. Both microbiological and biophysical techniques will be used to broadly test the role of CdrA in biofilm formation, and to investigate the roles of several predicted structural features of CdrA that likely are responsible for its role in the biofilm. Specifically, this hypothesis will be tested with two aims: (1) to examine the localization and functionality of CdrA and its cleavage products within P. aeruginosa biofilms using immunoblots, electron microscopy, and immunofluorescence; and (2) to investigate the structural motifs of CdrA that mediate its interactions with other biofilm matrix constituents as well as biotic surfaces such as respiratory epithelial cells using solid-state nuclear magnetic resonance (NMR), complementary bacterial genetics approaches, and CF host-molecule binding assays. The rationale for this research is that this improved understanding could provide a mechanism to control or treat biofilm-involved infections including CF lung infections. Furthermore, I seek to improve my knowledge and experimental skill-set of microbiology and biofilms in order to become a leader in biofilm and CF research, and to answer important questions about biofilm structure, function, and regulation that likely will rely upon a multidisciplinary approach.<\/p>\n<p>[\/et_pb_text][\/et_pb_column][\/et_pb_row][\/et_pb_section]<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Fellow: Courtney Reichhardt, PhD<br \/>\nMicrobiology<\/p>\n<p>Mentor: \u00a0Matthew Parsek, PhD<br \/>\nProfessor<br \/>\nMicrobiology<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_et_pb_use_builder":"on","_et_pb_old_content":"<p>P.I.: <a href=\"http:\/\/depts.washington.edu\/nephron\/directory\/bios\/deboer.html\" target=\"_blank\">Ian de boer, MD<\/a><br \/> Associate Professor of Medicine<br \/> Nephrology<\/p><p><a href=\"http:\/\/depts.washington.edu\/nephron\/directory\/bios\/kestenbaum.html\" target=\"_blank\">Bryan Kestenbaum, MD<\/a><br \/> Associate Professor of Medicine<br \/> Nephrology<\/p><p>Vitamin D deficiency is one of the most common nutritional deficits in cystic fibrosis (CF) patients, is resistant to treatment, and may contribute to bone disease and infections. Possible reasons for vitamin D deficiency in CF include intestinal malabsorption, altered liver metabolism, and loss of vital carrier proteins in the urine; however, empiric evidence to support these mechanisms is lacking.<\/p><p>In this application we propose a series of experiments designed to comprehensively define the vitamin D metabolic axis in CF. First, we will characterize the circulating profile of vitamin D metabolites, vitamin D carrier proteins, and downstream hormonal responses in 100 adult CF patients and 50 control subjects. Next we will conduct formal pharmacokinetic studies of radiolabeled tracer to probe the fate of substrate vitamin D in CF patients. We will then measure transcription of key vitamin D metabolism genes in circulating monocytes. Identifying the underlying causes of vitamin D deficiency in CF patients could suggest novel treatments that target vitamin D deficiency as a means to improve clinical outcomes in this disorder.<\/p>","_et_gb_content_width":"","_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":"","_links_to":"","_links_to_target":""},"categories":[18],"tags":[],"_links":{"self":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/1438"}],"collection":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/comments?post=1438"}],"version-history":[{"count":4,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/1438\/revisions"}],"predecessor-version":[{"id":1465,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/posts\/1438\/revisions\/1465"}],"wp:attachment":[{"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/media?parent=1438"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/categories?post=1438"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/depts.washington.edu\/cfrtc\/wp-json\/wp\/v2\/tags?post=1438"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}