Kenneth T. Appell
Researcher
Also affiliated: American Pharmacists Association (2009); United States Pharmacopeial Convention (2008–2009)
Unknown Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Kenneth T. Appell's research focuses on the molecular mechanisms of bacterial pathogens, particularly *Yersinia pestis*, the bacterium responsible for plague. His work investigates how these bacteria regulate the expression of virulence factors, such as pesticin and plasminogen activator protease. Appell has examined the role of specific bacterial proteins, like BipA, in modulating these factors and has explored the involvement of two-component regulatory systems, such as PhoP/PhoQ, in controlling their production.
His recent publications also delve into the host immune response to infection, specifically the contribution of pulmonary interleukin-17 to neutrophil infiltration during pneumonic plague. Appell's research network includes collaborators such as Madeleine G. Scott, Jon S. Blevins, and Wanfeng Guo from the University of Arkansas for Medical Sciences, with whom he has co-authored multiple publications.
Metrics
- h-index: 1
- Publications: 6
- Citations: 9
Selected Publications
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<i>Yersinia pestis</i> plasminogen activator protease is regulated by the PhoP/PhoQ two-component system (2025)
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<i>Yersinia pestis</i> BipA is a novel regulator of pesticin and a type 6 secretion system (2025)
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Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague (2023)
Collaboration Network
Top Collaborators
- Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague
- <i>Yersinia pestis</i> BipA is a novel regulator of pesticin and a type 6 secretion system
- <i>Yersinia pestis</i> plasminogen activator protease is regulated by the PhoP/PhoQ two-component system
- Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague
- <i>Yersinia pestis</i> BipA is a novel regulator of pesticin and a type 6 secretion system
- <i>Yersinia pestis</i> plasminogen activator protease is regulated by the PhoP/PhoQ two-component system
- <i>Yersinia pestis</i> BipA is a novel regulator of pesticin and a type 6 secretion system
- <i>Yersinia pestis</i> plasminogen activator protease is regulated by the PhoP/PhoQ two-component system
- <i>Yersinia pestis</i> BipA is a novel regulator of pesticin and a type 6 secretion system
- <i>Yersinia pestis</i> plasminogen activator protease is regulated by the PhoP/PhoQ two-component system
- Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague
- Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague
- Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague
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