{"id":{"repo_id":"columbus-state","oai_identifier":"oai:csuepress.columbusstate.edu:theses_dissertations-1311"},"canonical_url":"https://search.dev.ndltd.org/etd/columbus-state/oai:csuepress.columbusstate.edu:theses_dissertations-1311","repository":{"repo_id":"columbus-state","name":"Columbus State University","base_url":"https://csuepress.columbusstate.edu/do/oai/"},"display":{"title":"The Relationship Between Biofilm Production and Human Respiratory Cell Attachment and Invasion by Acinetobacter Baumannii","abstract":"<p><em>Acinetobacter baumannii</em> is an opportunistic gram-negative bacterial pathogen that causes many nosocomial infections in immunocompromised individuals. Common infections include catheter-associated urinary tract infections, ventilator-associated pneumonia, skin and soft tissue infections, and bloodstream infections that often lead to septicemia. Increasing multidrug resistance (MDR) in <em>A. baumannii</em> warrants new approaches to understanding its virulence mechanisms and pathogenicity. As a first step in infection, <em>A. baumannii</em> can attach to host cells, providing a surface for the bacteria to grow and perhaps facilitating biofilm formation and subsequent tissue invasion. In this study, we evaluated antibiotic resistance and characterized biofilm formation, attachment, invasion, and surface protein RNA transcription profiles of<em> A. baumannii</em> clinical isolates. Some isolates were resistant to commonly prescribed antibiotics, with six of the seventeen showing MDR. We found that 16 of the 17 strains produce biofilms in varying amounts; all strains were able to adhere to and invade A549 pulmonary cells in high levels; and some of the strains exhibited genes associated with biofilm formation, attachment, and invasion. Levels of biofilm formation, attachment to A549 cells, and invasion of A549 were not associated with the presence or absence of target genes <em>ompA, abaI, pga operon, bap, csuE, or blaPER-1</em>. Virulence of <em>A. baumannii</em> clinical isolates increases due to their ability to produce biofilms and to attach to and invade host cells. It is important to elucidate further mechanisms of virulence in order to better treat <em>A. baumannii</em> infections and to prevent transmission and future outbreaks. We aimed to elucidate new information on the pathogenicity of <em>A. baumannii</em> that could lead to new therapeutic treatments for these infections.</p>","abstract_html":"&lt;p&gt;&lt;em&gt;Acinetobacter baumannii&lt;/em&gt; is an opportunistic gram-negative bacterial pathogen that causes many nosocomial infections in immunocompromised individuals. Common infections include catheter-associated urinary tract infections, ventilator-associated pneumonia, skin and soft tissue infections, and bloodstream infections that often lead to septicemia. Increasing multidrug resistance (MDR) in &lt;em&gt;A. baumannii&lt;/em&gt; warrants new approaches to understanding its virulence mechanisms and pathogenicity. As a first step in infection, &lt;em&gt;A. baumannii&lt;/em&gt; can attach to host cells, providing a surface for the bacteria to grow and perhaps facilitating biofilm formation and subsequent tissue invasion. In this study, we evaluated antibiotic resistance and characterized biofilm formation, attachment, invasion, and surface protein RNA transcription profiles of&lt;em&gt; A. baumannii&lt;/em&gt; clinical isolates. Some isolates were resistant to commonly prescribed antibiotics, with six of the seventeen showing MDR. We found that 16 of the 17 strains produce biofilms in varying amounts; all strains were able to adhere to and invade A549 pulmonary cells in high levels; and some of the strains exhibited genes associated with biofilm formation, attachment, and invasion. Levels of biofilm formation, attachment to A549 cells, and invasion of A549 were not associated with the presence or absence of target genes &lt;em&gt;ompA, abaI, pga operon, bap, csuE, or blaPER-1&lt;/em&gt;. Virulence of &lt;em&gt;A. baumannii&lt;/em&gt; clinical isolates increases due to their ability to produce biofilms and to attach to and invade host cells. It is important to elucidate further mechanisms of virulence in order to better treat &lt;em&gt;A. baumannii&lt;/em&gt; infections and to prevent transmission and future outbreaks. We aimed to elucidate new information on the pathogenicity of &lt;em&gt;A. baumannii&lt;/em&gt; that could lead to new therapeutic treatments for these infections.&lt;/p&gt;","abstract_has_math":false,"creators":["Pearson, Rachel A."],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Dr. Lauren B. King","Dr. Kathleen Hughes","Dr. Elizabeth Klar"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2019,"date_issued":"2019-12-01T08:00:00Z","date_published":"2019-12-01T08:00:00Z","updated_at":"2026-07-24T01:45:01Z","subjects":["Acinetobacter Baumannii","Biofilm Formation","Attachment","Invasion","ompA","abaI","pga operon","bap","csuE","blaPER-1","Bacteria","Bacterial Infections and Mycoses","Biology","Immune System Diseases"],"languages":["English"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://csuepress.columbusstate.edu/theses_dissertations/309","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Dr. Lauren B. 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Common infections include catheter-associated urinary tract infections, ventilator-associated pneumonia, skin and soft tissue infections, and bloodstream infections that often lead to septicemia. Increasing multidrug resistance (MDR) in <em>A. baumannii</em> warrants new approaches to understanding its virulence mechanisms and pathogenicity. As a first step in infection, <em>A. baumannii</em> can attach to host cells, providing a surface for the bacteria to grow and perhaps facilitating biofilm formation and subsequent tissue invasion. In this study, we evaluated antibiotic resistance and characterized biofilm formation, attachment, invasion, and surface protein RNA transcription profiles of<em> A. baumannii</em> clinical isolates. Some isolates were resistant to commonly prescribed antibiotics, with six of the seventeen showing MDR. We found that 16 of the 17 strains produce biofilms in varying amounts; all strains were able to adhere to and invade A549 pulmonary cells in high levels; and some of the strains exhibited genes associated with biofilm formation, attachment, and invasion. Levels of biofilm formation, attachment to A549 cells, and invasion of A549 were not associated with the presence or absence of target genes <em>ompA, abaI, pga operon, bap, csuE, or blaPER-1</em>. Virulence of <em>A. baumannii</em> clinical isolates increases due to their ability to produce biofilms and to attach to and invade host cells. It is important to elucidate further mechanisms of virulence in order to better treat <em>A. baumannii</em> infections and to prevent transmission and future outbreaks. We aimed to elucidate new information on the pathogenicity of <em>A. baumannii</em> that could lead to new therapeutic treatments for these infections.</p>"]},{"key":"dc:title","label":"Title","values":["The Relationship Between Biofilm Production and Human Respiratory Cell Attachment and Invasion by Acinetobacter Baumannii"]}]}],"canonical_facts":{"dc:contributor":["Dr. Lauren B. King","Dr. Kathleen Hughes","Dr. Elizabeth Klar"],"dc:creator":["Pearson, Rachel A."],"dc:date.available":["2019-12-05T08:00:00Z"],"dc:description.abstract":["<p><em>Acinetobacter baumannii</em> is an opportunistic gram-negative bacterial pathogen that causes many nosocomial infections in immunocompromised individuals. Common infections include catheter-associated urinary tract infections, ventilator-associated pneumonia, skin and soft tissue infections, and bloodstream infections that often lead to septicemia. Increasing multidrug resistance (MDR) in <em>A. baumannii</em> warrants new approaches to understanding its virulence mechanisms and pathogenicity. As a first step in infection, <em>A. baumannii</em> can attach to host cells, providing a surface for the bacteria to grow and perhaps facilitating biofilm formation and subsequent tissue invasion. In this study, we evaluated antibiotic resistance and characterized biofilm formation, attachment, invasion, and surface protein RNA transcription profiles of<em> A. baumannii</em> clinical isolates. Some isolates were resistant to commonly prescribed antibiotics, with six of the seventeen showing MDR. We found that 16 of the 17 strains produce biofilms in varying amounts; all strains were able to adhere to and invade A549 pulmonary cells in high levels; and some of the strains exhibited genes associated with biofilm formation, attachment, and invasion. Levels of biofilm formation, attachment to A549 cells, and invasion of A549 were not associated with the presence or absence of target genes <em>ompA, abaI, pga operon, bap, csuE, or blaPER-1</em>. Virulence of <em>A. baumannii</em> clinical isolates increases due to their ability to produce biofilms and to attach to and invade host cells. It is important to elucidate further mechanisms of virulence in order to better treat <em>A. baumannii</em> infections and to prevent transmission and future outbreaks. We aimed to elucidate new information on the pathogenicity of <em>A. baumannii</em> that could lead to new therapeutic treatments for these infections.</p>"],"dc:identifier":["https://csuepress.columbusstate.edu/theses_dissertations/309"],"dc:language":["English"],"dc:subject":["Acinetobacter Baumannii","Biofilm Formation","Attachment","Invasion","ompA","abaI","pga operon","bap","csuE","blaPER-1","Bacteria","Bacterial Infections and Mycoses","Biology","Immune System Diseases"],"dc:title":["The Relationship Between Biofilm Production and Human Respiratory Cell Attachment and Invasion by Acinetobacter Baumannii"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T01:45:01Z"}