Porphyromonas gingivalis Manipulates Complement and TLR Signaling to Uncouple Bacterial Clearance from Inflammation and Promote Dysbiosis
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- 作者：Tomoki Maekawa1 ; 8 ; Jennifer L. Krauss2 ; 7 ; 8 ; Toshiharu Abe1 ; Ravi Jotwani2 ; Martha Triantafilou3 ; Kathy Triantafilou3 ; Ahmed Hashim4 ; Shifra Hoch5 ; Michael A. Curtis4 ; Gabriel Nussbaum5 ; John D. Lambris6 ; George Hajishengallis1 ; geoh@upenn.edu" class="auth_mail
- 刊名：Cell Host Microbe
- 出版年：11 June 2014
- 年：2014
- 卷：15
- 期：6
- 页码：768-778
- 全文大小：2300 K
文摘
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P. gingivalis degrades MyD88 and interferes with the neutrophil killing function
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P. gingivalis activates PI3K, which blocks phagocytosis and promotes inflammation
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These mechanisms require crosstalk between complement receptor C5aR and TLR2
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This crosstalk protects P. gingivalis and bystander bacteria and promotes dysbiosis