• 제목/요약/키워드: Fusobacterium animalis

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사람 치주염 병소의 치은연하지면세균막에서 분리된 Fusobacterium animalis KCOM 1280의 유전체 염기서열 해독 (Draft genome sequence of Fusobacterium animalis KCOM 1280 isolated from a human subgingival plaque of periodontitis lesion)

  • 박순낭;임윤경;신자영;노한성;국중기
    • 미생물학회지
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    • 제54권2호
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    • pp.146-148
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    • 2018
  • Fusobacterium animalis (예전에 Fusobacterium nucleatum subsp. animalis으로 알려짐)는 그람 음성이면서, 혐기성 및 선형의 세균이다. F. animalis는 사람 구강 내 정상 세균총의 하나이며 치주질환원인균이라 여겨지고 있다. F. animalis KCOM 1280 (= ChDC F318) 균주는 사람 치주질환 병소에서 분리되었다. 본 논문에서 F. animalis KCOM 1280 균주 유전체 염기서열을 해독하여 보고하고자 한다.

Anti-inflammatory, Antioxidant and Antimicrobial Effects of Artemisinin Extracts from Artemisia annua L.

  • Kim, Wan-Su;Choi, Woo Jin;Lee, Sunwoo;Kim, Woo Joong;Lee, Dong Chae;Sohn, Uy Dong;Shin, Hyoung-Shik;Kim, Wonyong
    • The Korean Journal of Physiology and Pharmacology
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    • 제19권1호
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    • pp.21-27
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    • 2015
  • The anti-inflammatory, antioxidant, and antimicrobial properties of artemisinin derived from water, methanol, ethanol, or acetone extracts of Artemisia annua L. were evaluated. All 4 artemisinin-containing extracts had anti-inflammatory effects. Of these, the acetone extract had the greatest inhibitory effect on lipopolysaccharide-induced nitric oxide (NO), prostaglandin $E_2$ ($PGE_2$), and proinflammatory cytokine ($IL-1{\beta}$, IL-6, and IL-10) production. Antioxidant activity evaluations revealed that the ethanol extract had the highest free radical scavenging activity, ($91.0{\pm}3.2%$), similar to ${\alpha}$-tocopherol (99.9%). The extracts had antimicrobial activity against the periodontopathic microorganisms Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum subsp. animalis, Fusobacterium nucleatum subsp. polymorphum, and Prevotella intermedia. This study shows that Artemisia annua L. extracts contain anti-inflammatory, antioxidant, and antimicrobial substances and should be considered for use in pharmaceutical products for the treatment of dental diseases.

A murine periodontitis model using coaggregation between human pathogens and a predominant mouse oral commensal bacterium

  • Liu, Mengmeng;Choi, Youngnim
    • Journal of Periodontal and Implant Science
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    • 제52권2호
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    • pp.141-154
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    • 2022
  • Purpose: C57BL/6 mice, which are among the most common backgrounds for genetically engineered mice, are resistant to the induction of periodontitis by oral infection with periodontal pathogens. This study aimed to develop a periodontitis model in C57BL/6 mice using coaggregation between human pathogens and the mouse oral commensal Streptococcus danieliae (Sd). Methods: The abilities of Porphyromonas gingivalis ATCC 33277 (Pg33277), P. gingivalis ATCC 49417 (Pg49417), P. gingivalis KUMC-P4 (PgP4), Fusobacterium nucleatum subsp. nucleatum ATCC 25586 (Fnn), and F. nucleatum subsp. animalis KCOM 1280 (Fna) to coaggregate with Sd were tested by a sedimentation assay. The Sd-noncoaggregating Pg33277 and 2 Sd-coaggregating strains, PgP4 and Fna, were chosen for animal experiments. Eighty C57BL/6 mice received oral gavage with Sd once and subsequently received vehicle alone (sham), Fna, Pg33277, PgP4, or Fna+PgP4 6 times at 2-day intervals. Mice were evaluated at 5 or 8 weeks after the first gavage of human strains. Results: Fnn, Fna, and PgP4 efficiently coaggregated with Sd, but Pg33277 and Pg49417 did not. Alveolar bone loss was significantly higher in the PgP4 group at both time points (weeks 5 and 8) and in all experimental groups at week 8 compared with the sham group. The PgP4 group presented greater alveolar bone loss than the other experimental groups at both time points. A higher degree of alveolar bone loss accompanied higher bacterial loads in the oral cavity, the invasion of not only PgP4 but also Sd and Fna, and the serum antibody responses to these bacteria. Conclusions: Periodontitis was successfully induced in C57BL/6 mice by oral infection with a P. gingivalis strain that persists in the oral cavity through coaggregation with a mouse oral commensal bacterium. This new model will be useful for studying the role of human oral bacteria-host interactions in periodontitis using genetically engineered mice.