Match tier Self-claimed
Presence Current · Arkansas
Last published 2025
Sources Self-reported
Refreshed 2026-10-03

Kenneth T. Appell

Identity verified by the researcher via institutional email.

Role not yet determined

1 h-index 5 pubs 9 cited

  • Yersinia pestis
  • Animals
  • Plague
  • Mice
  • Bacterial Proteins
  • Gene Expression Regulation, Bacterial
  • Type VI Secretion Systems
  • Virulence Factors
  • Pore Forming Cytotoxic Proteins
  • Plasminogen Activators
  • Disease Models, Animal
  • Lung
  • Mice, Inbred C57BL
  • Interleukin-17
  • Neutrophil Infiltration

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Biography and Research Information

OverviewAI-generated summary

Kenneth T. Appell's research focuses on the molecular mechanisms of bacterial pathogenesis, particularly concerning the bacterium *Yersinia pestis*, the causative agent of plague. His work investigates how *Yersinia pestis* interacts with host organisms and employs specific virulence factors to establish infection. Recent publications explore the role of the BipA protein as a regulator of pesticin and type VI secretion systems, as well as the regulation of the *Yersinia pestis* plasminogen activator protease by the PhoP/PhoQ two-component system. Additionally, his research has examined the contribution of pulmonary interleukin-17 to neutrophil infiltration during pneumonic plague. Appell collaborates with researchers at the University of Arkansas for Medical Sciences, including Madeleine G. Scott, Jon S. Blevins, and Wanfeng Guo, on shared publications.

Metrics

  • h-index: 1
  • Publications: 5
  • Citations: 9

Selected Publications

  • Yersinia pestis plasminogen activator protease is regulated by the PhoP/PhoQ two-component system (2025)
    Journal of Bacteriology DOI OpenAlex
  • Yersinia pestis BipA is a novel regulator of pesticin and a type 6 secretion system (2025)
    Infection and Immunity 1 citation DOI OpenAlex
  • Pulmonary Expression of Interleukin-17 Contributes to Neutrophil Infiltration into the Lungs during Pneumonic Plague (2023)
    Infection and Immunity 8 citations DOI OpenAlex

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Collaboration Network

7 Collaborators 3 Institutions 1 Country

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