Porphyromonas gingivalisis one of the most important bacterial etiological agents involved in adult periodontitis. It possesses several virulence factors which aid in its persistence in the periodontal pocket leading to the development of some systemic illnesses. As an anaerobe, P. gingivalismust employ mechanisms to avoid oxidative stress generated by reactive oxygen species during phagocytosis, or the occasional exposure to air. Presently, only three proteins with antioxidant enzymatic function have been identified as playing a role in oxidative stress resistance in P. gingivalis. In this study, attention was focused on the alkyl hydroperoxidase subunit C (ahpC)and bacterioferritin comigratory protein (bcp) genes, DNA repair mechanisms and the unique hemin layer of P. gingivalis. We tested the physiological function of the isogenic ahpC and bcpmutants to hydrogen peroxide. When compared to the wild-type P. gingivalis W83, both the ahpC and bcpisogenic mutants, designated FLL141 and FLL301 respectively, demonstrated a greater sensitivity to hydrogen peroxide. However when tested in an animal model of virulence, the virulence potential of these mutants was similar when compared to the wild-type. These data suggest an involvement of these genes in oxidative stress protection but not in virulence. Further, recent reports indicated that the hemin layer was involved in protecting P. gingivalisfrom hydrogen peroxide. Consequently, the hypothesis that a non-pigmented strain of P. gingivalis, FLL92, would be more sensitive to oxidative stress than the wild-type P. gingivalisW83 was investigated.
Interestingly, when compared to the parent strain, FLL92 was more resistant to hydrogen peroxide. As a result, the hypothesis that P. gingivalis FLL92 would incur more DNA damage than the wild-type was investigated. Data from these experiments demonstrated an increase in the oxidative DNA lesion 8-oxoguanine and its related enzymatic removal activity in P. gingivalis FLL92 in comparison with the parent strain. Additionally, a novel removal activity for 8-oxoguanine from duplex DNA was identified in P. gingivalis when compared to other oral anaerobes. Collectively, these data suggest that P. gingivalis W83 may utilize antioxidant enzymatic activity, the hemin layer and DNA repair enzymes as part of an intricate defense mechanism against oxidative stress.
","abstract_html":"<p><em>Porphyromonas gingivalis</em>is one of the most important bacterial etiological agents involved in adult periodontitis. It possesses several virulence factors which aid in its persistence in the periodontal pocket leading to the development of some systemic illnesses. As an anaerobe, <em>P. gingivalis</em>must employ mechanisms to avoid oxidative stress generated by reactive oxygen species during phagocytosis, or the occasional exposure to air. Presently, only three proteins with antioxidant enzymatic function have been identified as playing a role in oxidative stress resistance in <em>P. gingivalis.</em> In this study, attention was focused on the alkyl hydroperoxidase subunit C <em>(ahpC)</em>and bacterioferritin comigratory protein <em>(bcp)</em> genes, DNA repair mechanisms and the unique hemin layer of <em>P. gingivalis. </em>We tested the physiological function of the isogenic <em>ahpC</em> and <em>bcp</em>mutants to hydrogen peroxide. When compared to the wild-type <em>P. gingivalis</em> W83, both the <em>ahpC</em> and <em>bcp</em>isogenic mutants, designated FLL141 and FLL301 respectively, demonstrated a greater sensitivity to hydrogen peroxide. However when tested in an animal model of virulence, the virulence potential of these mutants was similar when compared to the wild-type. These data suggest an involvement of these genes in oxidative stress protection but not in virulence. Further, recent reports indicated that the hemin layer was involved in protecting <em>P. gingivalis</em>from hydrogen peroxide. Consequently, the hypothesis that a non-pigmented strain of <em>P. gingivalis</em>, FLL92, would be more sensitive to oxidative stress than the wild-type <em>P. gingivalis</em>W83 was investigated. </p> <p>Interestingly, when compared to the parent strain, FLL92 was more resistant to hydrogen peroxide. As a result, the hypothesis that <em>P. gingivalis</em> FLL92 would incur more DNA damage than the wild-type was investigated. Data from these experiments demonstrated an increase in the oxidative DNA lesion 8-oxoguanine and its related enzymatic removal activity in <em>P. gingivalis</em> FLL92 in comparison with the parent strain. Additionally, a novel removal activity for 8-oxoguanine from duplex DNA was identified in <em>P. gingivalis</em> when compared to other oral anaerobes. Collectively, these data suggest that <em>P. gingivalis</em> W83 may utilize antioxidant enzymatic activity, the hemin layer and DNA repair enzymes as part of an intricate defense mechanism against oxidative stress.</p>","abstract_has_math":false,"creators":["Johnson, Neal Antonio"],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Dissertation","degree_discipline":"Microbiology, Molecular Biology and Biochemistry","degree_department":null,"school":null,"contributors":["Hansel Fletcher","Carlos Casiano","Alan Escher","James Kettering","Lawrence C. Sowers"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2004,"date_issued":"2004-06-01T07:00:00Z","date_published":"2004-06-01T07:00:00Z","updated_at":"2026-07-24T02:53:08Z","subjects":["Microbiology","Porphyromonas gingivalis -- enzymology; Porphyromonas gingivalis -- genetics; Porphyromonas gingivalis -- pathogenicity; Oxidative Stress; Virulence; Gene Expression Regulation, Bacterial; Periodontitis -- microbiology."],"languages":["English"],"rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://scholarsrepository.llu.edu/etd/635","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Hansel Fletcher","Carlos Casiano","Alan Escher","James Kettering","Lawrence C. 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The author retains all other copyrights."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarsrepository.llu.edu/etd/635"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Porphyromonas gingivalisis one of the most important bacterial etiological agents involved in adult periodontitis. It possesses several virulence factors which aid in its persistence in the periodontal pocket leading to the development of some systemic illnesses. As an anaerobe, P. gingivalismust employ mechanisms to avoid oxidative stress generated by reactive oxygen species during phagocytosis, or the occasional exposure to air. Presently, only three proteins with antioxidant enzymatic function have been identified as playing a role in oxidative stress resistance in P. gingivalis. In this study, attention was focused on the alkyl hydroperoxidase subunit C (ahpC)and bacterioferritin comigratory protein (bcp) genes, DNA repair mechanisms and the unique hemin layer of P. gingivalis. We tested the physiological function of the isogenic ahpC and bcpmutants to hydrogen peroxide. When compared to the wild-type P. gingivalis W83, both the ahpC and bcpisogenic mutants, designated FLL141 and FLL301 respectively, demonstrated a greater sensitivity to hydrogen peroxide. However when tested in an animal model of virulence, the virulence potential of these mutants was similar when compared to the wild-type. These data suggest an involvement of these genes in oxidative stress protection but not in virulence. Further, recent reports indicated that the hemin layer was involved in protecting P. gingivalisfrom hydrogen peroxide. Consequently, the hypothesis that a non-pigmented strain of P. gingivalis, FLL92, would be more sensitive to oxidative stress than the wild-type P. gingivalisW83 was investigated.
Interestingly, when compared to the parent strain, FLL92 was more resistant to hydrogen peroxide. As a result, the hypothesis that P. gingivalis FLL92 would incur more DNA damage than the wild-type was investigated. Data from these experiments demonstrated an increase in the oxidative DNA lesion 8-oxoguanine and its related enzymatic removal activity in P. gingivalis FLL92 in comparison with the parent strain. Additionally, a novel removal activity for 8-oxoguanine from duplex DNA was identified in P. gingivalis when compared to other oral anaerobes. Collectively, these data suggest that P. gingivalis W83 may utilize antioxidant enzymatic activity, the hemin layer and DNA repair enzymes as part of an intricate defense mechanism against oxidative stress.
"]},{"key":"dc:title","label":"Title","values":["Mechanisms of Oxidative Stress Resistance in Porphyromonas gingivalis W83"]}]}],"canonical_facts":{"dc:contributor":["Hansel Fletcher","Carlos Casiano","Alan Escher","James Kettering","Lawrence C. Sowers"],"dc:creator":["Johnson, Neal Antonio"],"dc:description.abstract":["Porphyromonas gingivalisis one of the most important bacterial etiological agents involved in adult periodontitis. It possesses several virulence factors which aid in its persistence in the periodontal pocket leading to the development of some systemic illnesses. As an anaerobe, P. gingivalismust employ mechanisms to avoid oxidative stress generated by reactive oxygen species during phagocytosis, or the occasional exposure to air. Presently, only three proteins with antioxidant enzymatic function have been identified as playing a role in oxidative stress resistance in P. gingivalis. In this study, attention was focused on the alkyl hydroperoxidase subunit C (ahpC)and bacterioferritin comigratory protein (bcp) genes, DNA repair mechanisms and the unique hemin layer of P. gingivalis. We tested the physiological function of the isogenic ahpC and bcpmutants to hydrogen peroxide. When compared to the wild-type P. gingivalis W83, both the ahpC and bcpisogenic mutants, designated FLL141 and FLL301 respectively, demonstrated a greater sensitivity to hydrogen peroxide. However when tested in an animal model of virulence, the virulence potential of these mutants was similar when compared to the wild-type. These data suggest an involvement of these genes in oxidative stress protection but not in virulence. Further, recent reports indicated that the hemin layer was involved in protecting P. gingivalisfrom hydrogen peroxide. Consequently, the hypothesis that a non-pigmented strain of P. gingivalis, FLL92, would be more sensitive to oxidative stress than the wild-type P. gingivalisW83 was investigated.
Interestingly, when compared to the parent strain, FLL92 was more resistant to hydrogen peroxide. As a result, the hypothesis that P. gingivalis FLL92 would incur more DNA damage than the wild-type was investigated. Data from these experiments demonstrated an increase in the oxidative DNA lesion 8-oxoguanine and its related enzymatic removal activity in P. gingivalis FLL92 in comparison with the parent strain. Additionally, a novel removal activity for 8-oxoguanine from duplex DNA was identified in P. gingivalis when compared to other oral anaerobes. Collectively, these data suggest that P. gingivalis W83 may utilize antioxidant enzymatic activity, the hemin layer and DNA repair enzymes as part of an intricate defense mechanism against oxidative stress.
"],"dc:identifier":["https://scholarsrepository.llu.edu/etd/635"],"dc:language":["English"],"dc:rights":["This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights."],"dc:subject":["Microbiology","Porphyromonas gingivalis -- enzymology; Porphyromonas gingivalis -- genetics; Porphyromonas gingivalis -- pathogenicity; Oxidative Stress; Virulence; Gene Expression Regulation, Bacterial; Periodontitis -- microbiology."],"dc:title":["Mechanisms of Oxidative Stress Resistance in Porphyromonas gingivalis W83"],"thesis:degree_discipline":["Microbiology, Molecular Biology and Biochemistry"],"thesis:degree_level":["Dissertation"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T02:53:08Z"}