ポリマー型免疫グロブリン受容体は,ヒト鼻上皮細胞に肺炎球菌を転移させます
J R Zhang1, K E Mostov, M E Lamm
1Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Cell
|October 13, 2000
まとめ
ヒトポリマー免疫グロブリン受容体 (hpIgR) は,肺炎球菌CbpAに結合し,細菌の結合と侵入を強化する. この相互作用は,病原体が宿主粘膜の免疫メカニズムを感染のためにどのように利用するかを強調しています.
科学分野:
- 免疫学 免疫学とは
- 微生物学 微生物学とは
- 細胞生物学 細胞生物学
背景:
- ポリマー免疫グロブリン受容体 (pIgR) は粘膜免疫に不可欠であり,ポリマー免疫グロブリン (pIg) を上皮の障壁を越えて輸送する.
- 微生物の病原体は,しばしば宿主細胞の機械を併用して,感染と植民を容易にする.
研究 の 目的:
- ヒトのポリメリック免疫グロブリン受容体 (hpIgR) と,Streptococcus pneumoniae.e.との相互作用を調査する.
- hpIgRが肺炎球菌の粘着と粘膜表面への侵入を促進するかどうかを判断する.
主な方法:
- 同免疫プレシピテーション測定法では,hpIgRと肺炎球菌アデシンCbpAとの結合を評価する.
- 人間の鼻臓細胞と,hpIgR.を発現するMDCK細胞を用いた細胞培養実験.
- hpIgR,CbpA,および特定の抗体の存在または欠如において,肺炎球菌の粘着および侵入を評価する.
主要な成果:
- 人間のpIgR (hpIgR) は,肺炎球菌アデシンCbpA.に直接結合する.
- hpIgRの発現は,細胞モデルにおける肺炎球菌の粘着と侵入を著しく強化する.
- hpIgR-CbpAの相互作用が遺伝的ノックアウトまたは抗体によって破壊された場合,この強化は廃止されます.
- ウサギのpIgR (rpIgR) はCbpAと結合せず,肺炎球菌の転移を促進しない.
結論:
- 肺炎菌はCbpAアデシンを利用してhpIgRと相互作用する.
- この相互作用は,粘膜上皮質に肺炎球菌の転移を促進し,新しい病原性メカニズムを表します.
- hpIgR媒介のトランサイトシスは,肺炎球菌感染症を予防するための標的となる経路です.
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