Michael A. Curtis
King's College London
139 Papers
1.7K Citations
Michael A. Curtis is an academic researcher from King's College London. The author has contributed to research in topics: Porphyromonas gingivalis & Biology. The author has an hindex of 55, co-authored 132 publications. Previous affiliations of Michael A. Curtis include Queen Mary University of London & University of London.
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Papers
The keystone-pathogen hypothesis
TL;DR: Critical assessment of the available literature that supports the keystone-pathogen hypothesis holds that certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodelling a normally benign microbiota into a dysbiotic one.
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Low-Abundance Biofilm Species Orchestrates Inflammatory Periodontal Disease through the Commensal Microbiota and Complement
George Hajishengallis,Shuang Liang,Mark A. Payne,Ahmed Hashim,Ravi Jotwani,Mehmet A. Eskan,Megan L. McIntosh,Asil Alsam,Keith L. Kirkwood,John D. Lambris,Richard P. Darveau,Michael A. Curtis +11 more
TL;DR: It is shown that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss, demonstrating that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease.
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The role of the microbiota in periodontal disease.
TL;DR: Despite clear insights into both sides of the host/microbe balance in periodontal disease, there remain several unresolved issues concerning the role of the microbiota in disease.
537
Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer's disease brain tissue.
TL;DR: It is confirmed that LPS from periodontal bacteria can access the AD brain during life as labeling in the corresponding controls, with equivalent/longer postmortem interval, was absent.
512
Porphyromonas gingivalis as a Potential Community Activist for Disease
TL;DR: In a mouse model of periodontitis, it has been shown that modulation of complement function by P. gingivalis facilitates a significant change in both the amount and composition of the normal oral microbiotia, and this may represent one mechanism by whichperiodontitis can be initiated.
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