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  1. 学位論文
  2. 博士論文(医学)
  3. 本文

Nontypeable Haemophilus influenzae exploits the interaction between protein-E and vitronectin for the adherence and invasion to bronchial epithelial cells

http://hdl.handle.net/10271/3140
http://hdl.handle.net/10271/3140
0e6487b6-fa13-4929-a4b2-ec5fe50ef123
名前 / ファイル ライセンス アクション
DT_718ronbun.pdf 論文本文 (5.4 MB)
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Item type 学位論文 / Thesis or Dissertation(1)
公開日 2017-01-28
タイトル
タイトル Nontypeable Haemophilus influenzae exploits the interaction between protein-E and vitronectin for the adherence and invasion to bronchial epithelial cells
言語 en
言語
言語 eng
キーワード
主題 Haemophilus influenzae
キーワード
主題 NTHi
キーワード
主題 Intracellular invasion
キーワード
主題 Protein-E
キーワード
主題 Vitronectin
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_db06
資源タイプ doctoral thesis
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
その他のタイトル
その他のタイトル 無莢膜型ヘモフィルスインフルエンザ菌は気管支上皮細胞への接着と侵入にProtein-Eとビトロネクチンの相互作用を利用する
著者 Ikeda, Masaki

× Ikeda, Masaki

en Ikeda, Masaki

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書誌情報 en : BMC Microbiology

巻 15, p. 263, 発行日 2015-11-14
出版者
出版者 BioMed Central
言語 en
抄録
内容記述タイプ Abstract
内容記述 Background: Nontypeable Haemophilus influenzae (NTHi) is one of the most common Gram-negative pathogens in otitis media and exacerbation of chronic obstructive pulmonary disease. NTHi has been reported to invade bronchial epithelial cells. This penetration enables NTHi to evade the host immune system and antibiotics, and it seems to be related to the intractable features of these diseases. However, the precise mechanism of the invasion has been unknown. We hypothesized that protein-E, an outer membrane protein of NTHi, plays a role in this penetration into bronchial epithelial cells.
Results: We utilized two NTHi strains. NTHi efficiently attached to plate-bound vitronectin (254-309 / field at 1,000× magnification) and this attachment was blocked by pretreatment with protein-E peptide (PE84-108). The blockade of adhesion was dependent on the concentration of PE84-108. NTHi strains invaded bronchial epithelial cells and the intracellular bacteria were localized in early endosomes. Furthermore, intracellular invasion of NTHi was also blocked by PE84-108, but not by Arg-Gly-Asp (RGD) peptide. Pretreatment with PE84-108 significantly prevented cells from being invaded by both NTHi strains, which was confirmed by fluorescent microscope observation. In addition, pretreatment with PE84-108 significantly reduced percentages of CFU after gentamicin treatment of cells per input CFU.
Conclusions: These results suggest that NTHi does not directly bind to the cell surface, but binds to host vitronectin that is bound to the cell surface, via bacterial protein-E. Bacterial protein-E and host vitronectin play a role in the attachment to bronchial epithelial cells and is also involved in the subsequent intracellular invasion of NTHi. A novel vaccine or treatment strategy targeting the protein-E-vitronectin axis may prevent respiratory intracellular infection of NTHi and may lead to better clinical outcomes.
言語 en
学位名
学位名 博士(医学)
学位の区分
内容記述 doctoral
学位の分野
内容記述 医学系研究科
学位授与機関
学位授与機関識別子Scheme kakenhi
学位授与機関識別子 13802
学位授与機関名 浜松医科大学
学位授与年月日
学位授与年月日 2016-03-14
学位授与番号
学位授与番号 甲第718号
EISSN
収録物識別子タイプ EISSN
収録物識別子 1471-2180
PubMed番号
識別子タイプ PMID
関連識別子 26572616
出版社DOI
識別子タイプ DOI
関連識別子 https://doi.org/10.1186/s12866-015-0600-8
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
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